General paresis, also known as general paralysis of the insane (GPI), paralytic dementia, or syphilitic paresis is a severe neuropsychiatric disorder, classified as an organic mental disorder and is caused by late-stage syphilis and the chronic meningoencephalitis and cerebral atrophy that are associated with this late stage of the disease when left untreated. GPI differs from mere paresis, as mere paresis can result from multiple other causes and usually does not affect cognitive function. Degenerative changes caused by GPI are associated primarily with the frontal and temporal lobar cortex. The disease affects approximately 7% of individuals infected with syphilis, and is far more common in third world countries where fewer options for timely treatment are available. It is more common among men.
GPI was originally considered to be a type of madness due to a dissolute character, when first identified in the early 19th century. The condition’s connection with syphilis was discovered in the late 1880s. Progressively, with the discovery of organic arsenicals such as Salvarsan and Neosalvarsan (1910s), the development of pyrotherapy (1920s; a method of raising body temperature or sustaining an elevated body temperature using a fever), and the widespread availability and use of penicillin in the treatment of syphilis (1940s), the condition was rendered avoidable and curable. Prior to this, GPI was inevitably fatal, and it accounted for as much as 25% of the primary diagnoses for residents in public psychiatric hospitals.
While retrospective studies have found earlier instances of what may have been the same disorder, the first clearly identified examples of paresis among the insane were described in Paris after the Napoleonic Wars. General paresis of the insane was first described as a distinct disease in 1822 by Antoine Laurent Jesse Bayle. General paresis most often struck people (men far more frequently than women) between 20 and 40 years of age. By 1877, for example, the superintendent of an asylum for men in New York reported that in his institution this disorder accounted for more than 12% of admissions and more than 2% of deaths.
Originally, the cause was believed to be an inherent weakness of character or constitution. While Friedrich von Esmarch and the psychiatrist Peter Willers Jessen (junior) had asserted as early as 1857 that syphilis caused general paresis (progressive Paralyse), progress toward the general acceptance by the medical community of this idea was only accomplished later by the eminent 19th Century syphilographer Jean Alfred Fournier (1832—1914). In 1913 all doubt about the syphilitic nature of paresis was finally eliminated when Hideyo Noguchi and J. W. Moore demonstrated the syphilitic spirochaetes in the brains of paretics.
In 1917 Julius Wagner-Jauregg discovered that malaria therapy (in this case, medical induction of a fever) involving infecting paretic patients with malaria could halt the progression of general paresis. He won a Nobel Prize for this discovery in 1927. After World War II the use of penicillin to treat syphilis made general paresis a rarity: even patients manifesting early symptoms of actual general paresis were capable of full recovery with a course of penicillin. The disorder is now virtually unknown outside developing countries, and even there the epidemiology is substantially reduced.
Some notable cases of general paresis:
General Ranald S. Mackenzie was retired from the US Army in 1884 for “general paresis of the insane” 5 years before his death in 1889.
Theo Van Gogh, brother of painter Vincent van Gogh, died six months after Vincent in 1891 from “dementia parylitica” or what is now called syphilitic paresis.
The Chicago gangster Al Capone died of syphilitic paresis, having contracted syphilis in a brothel in 1919, and not having been properly treated for it in time to prevent his later onset of syphilitic paresis.
Signs and Symptoms
Symptoms of the disease first appear from 10 to 30 years after infection. Incipient GPI is usually manifested by neurasthenic difficulties, such as fatigue, headaches, insomnia, dizziness, etc. As the disease progresses, mental deterioration and personality changes occur. Typical symptoms include loss of social inhibitions, asocial behaviour, gradual impairment of judgment, concentration and short-term memory, euphoria, mania, depression, or apathy. Subtle shivering, minor defects in speech and Argyll Robertson pupil may become noticeable.
Delusions, common as the illness progresses, tend to be poorly systematized and absurd. They can be grandiose, melancholic, or paranoid. These delusions include ideas of great wealth, immortality, thousands of lovers, unfathomable power, apocalypsis, nihilism, self-guilt, self-blame, or bizarre hypochondriacal complaints. Later, the patient experiences dysarthria, intention tremors, hyperreflexia, myoclonic jerks, confusion, seizures and severe muscular deterioration. Eventually, the paretic dies bedridden, cachectic and completely disoriented, frequently in a state of status epilepticus.
The diagnosis could be differentiated from other known psychoses and dementias by a characteristic abnormality in eye pupil reflexes (Argyll Robertson pupil), and, eventually, the development of muscular reflex abnormalities, seizures, memory impairment (dementia) and other signs of relatively pervasive neurocerebral deterioration. Definitive diagnosis is based on the analysis of cerebrospinal fluid and tests for syphilis.
Although there were recorded cases of remission of the symptoms, especially if they had not passed beyond the stage of psychosis, these individuals almost invariably experienced relapse within a few months to a few years. Otherwise, the patient was seldom able to return home because of the complexity, severity and unmanageability of the evolving symptom picture. Eventually, the patient would become completely incapacitated, bed ridden, and would die, the process taking about three to five years on average.
Global mental health is the international perspective on different aspects of mental health. It is ‘the area of study, research and practice that places a priority on improving mental health and achieving equity in mental health for all people worldwide’. There is a growing body of criticism of the global mental health movement, and has been widely criticised as a neo-colonial or “missionary” project and as primarily a front for pharmaceutical companies seeking new clients for psychiatric drugs.
In theory, taking into account cultural differences and country-specific conditions, it deals with the epidemiology of mental disorders in different countries, their treatment options, mental health education, political and financial aspects, the structure of mental health care systems, human resources in mental health, and human rights issues among others.
The overall aim of the field of global mental health is to strengthen mental health all over the world by providing information about the mental health situation in all countries, and identifying mental health care needs in order to develop cost-effective interventions to meet those specific needs.
The Global Burden of Disease
Mental, neurological, and substance use disorders make a substantial contribution to the global burden of disease (GBD). This is a global measure of so-called disability-adjusted life years (DALY’s) assigned to a certain disease/disorder, which is a sum of the years lived with disability and years of life lost due to this disease within the total population. Neuropsychiatric conditions account for 14% of the global burden of disease. Among non-communicable diseases, they account for 28% of the DALY’s – more than cardiovascular disease or cancer. However, it is estimated that the real contribution of mental disorders to the global burden of disease is even higher, due to the complex interactions and co-morbidity of physical and mental illness.
Around the world, almost one million people die due to suicide every year, and it is the third leading cause of death among young people. The most important causes of disability due to health-related conditions worldwide include unipolar depression, alcoholism, schizophrenia, bipolar depression and dementia. In low- and middle-income countries, these conditions represent a total of 19.1% of all disability related to health conditions.
Mental Health by Country
The following is an outline from selected countries.
Mental illnesses and mental health disorders are widespread concerns among underdeveloped African countries, yet these issues are largely neglected, as mental health care in Africa is given statistically less attention than it is in other, westernised nations. Rising death tolls due to mental illness demonstrate the imperative need for improved mental health care policies and advances in treatment for Africans suffering from psychological disorders.
Underdeveloped African countries are so visibly troubled by physical illnesses, disease, malnutrition, and contamination that the dilemma of lacking mental health care has not been prioritised, makes it challenging to have a recognised impact on the African population. In 1988 and 1990, two original resolutions were implemented by the World Health Organisation’s (WHO) Member States in Africa. AFR/RC39/R1 and AFR/RC40/R9 attempted to improve the status of mental health care in specific African regions to combat its growing effects on the African people. However, it was found that these new policies had little impact on the status of mental health in Africa, ultimately resulting in an incline in psychological disorders instead of the desired decline, and causing this to seem like an impossible problem to manage.
In Africa, many socio-cultural and biological factors have led to heightened psychological struggles, while also masking their immediate level of importance to the African eye. Increasing rates of unemployment, violence, crime, rape, and disease are often linked to substance abuse, which can cause mental illness rates to inflate. Additionally, physical disease like HIV/AIDS, the Ebola epidemic, and malaria often have lasting psychological effects on victims that go unrecognised in African communities because of their inherent cultural beliefs. Traditional African beliefs have led to the perception of mental illness as being caused by supernatural forces, preventing helpful or rational responses to abnormal behaviour. For example, Ebola received loads of media attention when it became rampant in Africa and eventually spread to the US, however, researchers never really paid attention to its psychological effects on the African brain. Extreme anxiety, struggles with grief, feelings of rejection and incompetence, depression leading to suicide, PTSD, and much more are only some of the noted effects of diseases like Ebola. These epidemics come and go, but their lasting effects on mental health are remaining for years to come, and even ending lives because of the lack of action. There has been some effort to financially fund psychiatric support in countries like Liberia, due to its dramatic mental health crisis after warfare, but not much was benefited. Aside from financial reasons, it is so difficult to enforce mental health interventions and manage mental health in general in underdeveloped countries simply because the individuals living there do not necessarily believe in western psychiatry. It is also important to note that the socio-cultural model of psychology and abnormal behaviour is dependent on factors surrounding cultural differences. This causes mental health abnormalities to remain more hidden due to the culture’s natural behaviour, compared to westernised behaviour and cultural norms.
This relationship between mental and physical illness is an ongoing cycle that has yet to be broken. While many organisations are attempting to solve problems about physical health in Africa, as these problems are clearly visible and recognisable, there is little action taken to confront the underlying mental effects that are left on the victims. It is recognised that many of the mentally ill in Africa search for help from spiritual or religious leaders, however this is widely because many African countries are significantly lacking in mental health professionals in comparison to the rest of the world. In Ethiopia alone, there are “only 10 psychiatrists for the population of 61 million people,” studies have shown. While numbers have definitely changed since this research was done, the lack of psychological professionals throughout African continues with a current average of 1.4 mental health workers per 100,000 people compared to the global statistic of 9.0 professionals per 100,00 people. Additionally, statistics show that the “global annual rate of visits to mental health outpatient facilities is 1,051 per 100,000 population,” while “in Africa the rate is 14 per 100,000” visits. About half of Africa’s countries have some sort of mental health policy, however, these policies are highly disregarded, as Africa’s government spends “less than 1% of the total health budget on mental health”. Specifically in Sierra Leone, about 98.8% of people suffering from mental disorders remain untreated, even after the building of a well below average psychiatric hospital, further demonstrating the need for intervention.
Not only has there been little hands-on action taken to combat mental health issues in Africa, but there has also been little research done on the topic to spread its awareness and prevent deaths. The Lancet Global Health acknowledges that there are well over 1,000 published articles covering physical health in Africa, but there are still less than 50 discussing mental health. And this pressing dilemma of prioritising physical health vs. mental health is only worsening as the continent’s population is substantially growing with research showing that “Between 2000 and 2015 the continent’s population grew by 49%, yet the number of years lost to disability as a result of mental and substance use disorders increased by 52%”. The number of deaths caused by mental instability is truly competing with those caused by physical diseases: “In 2015, 17.9 million years were lost to disability as a consequence of mental health problems. Such disorders were almost as important a cause of years lost to disability as were infectious and parasitic diseases, which accounted for 18.5 million years lost to disability,”. Mental health and physical health care, while they may seem separate, are very much connected, as these two factors determine life or death for humans. As new challenges surface and old challenges still haven’t been prioritised, Africa’s mental health care policies need significant improvement in order to provide its people with the appropriate health care they deserve, hopefully preventing this problem from expanding.
A survey conducted by Australian Bureau of Statistics in 2008 regarding adults with manageable to severe neurosis reveals almost half of the population had a mental disorder at some point of their life and one in five people had a sustained disorder in the preceding 12 months. In neurotic disorders, 14% of the population experienced anxiety and comorbidity disorders were next to common mental disorder with vulnerability to substance abuse and relapses. There were distinct gender differences in disposition to mental health illness. Women were found to have high rate of mental health disorders, and Men had higher propensity of risk for substance abuse. The SMHWB survey showed families that had low socioeconomic status and high dysfunctional patterns had a greater proportional risk for mental health disorders. A 2010 survey regarding adults with psychosis revealed 5 persons per 1,000 in the population seeks professional mental health services for psychotic disorders and the most common psychotic disorder was schizophrenia.
Mental health disorder is considered a major public health concern and it constitutes about 13% of the Global Burden of disease and severe mental health disease may reduce each individual’s life expectancy by about 20%. Low and middle-income countries have a higher burden of mental health disorder as it is not considered as a health problem as other chronic diseases. Being a low-income country, in Bangladesh, mental health issues are highly stigmatised.
A community-based study in the rural area of Bangladesh in 2000-2001 estimated that the burden of mental morbidity was 16.5% among rural people and most were suffering from mainly depression and anxiety and which was one-half and one-third of total cases respectively. Furthermore, the prevalence of mental disorders was higher in women in large families aged 45 years.
Care for mental health in Bangladesh
A study conducted in 2008 stated that only 16% of patients came directly to the Mental Health Practitioner with a mean delay of 10.5 months of the onset of mental illness, which made them more vulnerable in many ways. 22% of patients went for the religious or traditional healer and 12% consulted a rural medical practitioner with the least delay of 2-2.5 weeks.
According to statistics released by the Centre of Addiction and Mental Health one in five people in Canada experience a mental health or addiction problem. Young people of ages 15 to 25 are particularly found to be vulnerable. Major depression is found to affect 8% and anxiety disorder 12% of the population. Women are 1.5 times more likely to suffer from mood and anxiety disorders. WHO points out that there are distinct gender differences in patterns of mental health and illness. The lack of power and control over their socioeconomic status, gender based violence; low social position and responsibility for the care of others render women vulnerable to mental health risks. Since more women than men seek help regarding a mental health problem, this has led to not only gender stereotyping but also reinforcing social stigma. WHO has found that this stereotyping has led doctors to diagnose depression more often in women than in men even when they display identical symptoms. Often communication between health care providers and women is authoritarian leading to either the under-treatment or over-treatment of these women.
Women’s College Hospital has a program called the “Women’s Mental Health Program” where doctors and nurses help treat and educate women regarding mental health collaboratively, individually, and online by answering questions from the public.
Another Canadian organisation serving mental health needs is the Centre for Addiction and Mental Health (CAMH). CAMH is one of Canada’s largest and most well-known health and addiction facilities, and it has received international recognitions from the Pan American Health Organisation and WHO Collaborating Centre. They do research in areas of addiction and mental health in both men and women. In order to help both men and women, CAMH provides “clinical care, research, education, policy development and health promotion to help transform the lives of people affected by mental health and addiction issues.” CAMH is different from Women’s College Hospital due to its widely known rehab centre for women who have minor addiction issues, to severe ones. This organization provides care for mental health issues by assessments, interventions, residential programs, treatments, and doctor and family support.
In Israel, a Mental Health Insurance Reform took effect in July 2015, transferring responsibility for the provision of mental health services from the Ministry of Health to the four national health plans. Physical and mental health care were united under one roof; previously they had functioned separately in terms of finance, location, and provider. Under the reform, the health plans developed new services or expanded existing ones to address mental health problems.
According to the WHO in 2004, depression is the leading cause of disability in the United States for individuals ages 15 to 44. Absence from work in the US due to depression is estimated to be in excess of $31 billion per year. Depression frequently co-occurs with a variety of medical illnesses such as heart disease, cancer, and chronic pain and is associated with poorer health status and prognosis. Each year, roughly 30,000 Americans take their lives, while hundreds of thousands make suicide attempts. In 2004, suicide was the 11th leading cause of death in the United States, third among individuals ages 15-24. Despite the increasingly availability of effectual depression treatment, the level of unmet need for treatment remains high. By way of comparison, a study conducted in Australia during 2006 to 2007 reported that one-third (34.9%) of patients diagnosed with a mental health disorder had presented to medical health services for treatment. The US has a shortage of mental healthcare workers, contributing to the unmet need for treatment. By 2025, the US will need an additional 15,400 psychiatrists and 57,490 psychologists to meet the demand for treatment.
It is estimated that one in four people in the world will be affected by mental or neurological disorders at some point in their lives. Although many effective interventions for the treatment of mental disorders are known, and awareness of the need for treatment of people with mental disorders has risen, the proportion of those who need mental health care but who do not receive it remains very high. This so-called “treatment gap” is estimated to reach between 76-85% for low- and middle-income countries, and 35-50% for high-income countries.
Despite the acknowledged need, for the most part there have not been substantial changes in mental health care delivery during the past years. Main reasons for this problem are public health priorities, lack of a mental health policy and legislation in many countries, a lack of resources – financial and human resources – as well as inefficient resource allocation.
In 2011, the WHO estimated a shortage of 1.18 million mental health professionals, including 55,000 psychiatrists, 628,000 nurses in mental health settings, and 493,000 psychosocial care providers needed to treat mental disorders in 144 low- and middle-income countries. The annual wage bill to remove this health workforce shortage was estimated at about US$4.4 billion.
Information and evidence about cost-effective interventions to provide better mental health care are available. Although most of the research (80%) has been carried out in high-income countries, there is also strong evidence from low- and middle-income countries that pharmacological and psychosocial interventions are effective ways to treat mental disorders, with the strongest evidence for depression, schizophrenia, bipolar disorder and hazardous alcohol use.
Recommendations to strengthen mental health systems around the world have been first mentioned in the WHO’s World Health Report 2001, which focused on mental health:
Provide treatment in primary care.
Make psychotropic drugs available.
Give care in the community.
Educate the public.
Involve communities, families and consumers.
Establish national policies, programs and legislation.
Develop human resources.
Link with other sectors.
Monitor community mental health.
Support more research.
Based on the data of 12 countries, assessed by the WHO Assessment Instrument for Mental Health Systems (WHO-AIMS), the costs of scaling up mental health services by providing a core treatment package for schizophrenia, bipolar affective disorder, depressive episodes and hazardous alcohol use have been estimated. Structural changes in mental health systems according to the WHO recommendations have been taken into account.
For most countries, this model suggests an initial period of investment of US$0.30 – 0.50 per person per year. The total expenditure on mental health would have to rise at least ten-fold in low-income countries. In those countries, additional financial resources will be needed, while in middle- and high-income countries the main challenge will be the reallocation of resources within the health system to provide better mental health service.
Prevention is beginning to appear in mental health strategies, including the 2004 WHO report “Prevention of Mental Disorders”, the 2008 EU “Pact for Mental Health” and the 2011 US National Prevention Strategy. NIMH or the National Institute of Mental Health has over 400 grants.
World Health Organisation (WHO)
Two of WHO’s core programmes for mental health are WHO MIND (Mental health improvements for Nations Development) and Mental Health Gap Action Programme (mhGAP).
WHO MIND focuses on 5 areas of action to ensure concrete changes in people’s daily lives. These are:
Action in and support to countries to improve mental health, such as the WHO Pacific Island Mental Health network (PIMHnet).
Mental health policy, planning and service development.
Mental health human rights and legislation.
Mental health as a core part of human development.
The QualityRights Project which works to unite and empower people to improve the quality of care and promote human rights in mental health facilities and social care homes.
Mental Health Gap Action Programme (mhGAP) is WHO’s action plan to scale up services for mental, neurological and substance use disorders for countries especially with low and lower middle incomes. The aim of mhGAP is to build partnerships for collective action and to reinforce the commitment of governments, international organisations and other stakeholders.
The mhGAP Intervention Guide (mhGAP-IG) was launched in October 2010. It is a technical tool for the management of mental, neurological and substance use disorders in non-specialist health settings. The priority conditions included are: depression, psychosis, bipolar disorders, epilepsy, developmental and behavioural disorders in children and adolescents, dementia, alcohol use disorders, drug use disorders, self-harm/suicide and other significant emotional or medically unexplained complaints.
This book charts the creeping of psychology and psychiatry across the borders of everyday experience and across geographical borders, as a form of colonialism that comes from within and from outside, swallowed in the form of a pill. It maps an anxious space where socio-economic crises come to be reconfigured as individual crisis – as ‘mental illness’; and how potentially violent interventions come to be seen as ‘essential’ treatment.
Another prominent critic is Ethan Watters, author of Crazy Like Us: The Globalisation of the American Psyche. A more constructive approach is offered by Vincenzo Di Nicola whose article on the Global South as an emergent epistemology creates a bridge between critiques of globalisation and the initial gaps and limitations of the Global Mental Health movement.
Catatonia is a neuropsychiatric behavioural syndrome that is characterised by abnormal movements, immobility, abnormal behaviours, and withdrawal. The onset of catatonia can be acute or subtle and symptoms can wax, wane, or change during episodes. There are several subtypes of catatonia: akinetic catatonia, excited catatonia, malignant catatonia, and other forms.
Although catatonia has historically been related to schizophrenia (catatonic schizophrenia), catatonia is most often seen in mood disorders. It is now known that catatonic symptoms are nonspecific and may be observed in other mental, neurologic, and medical conditions. Catatonia is not a stand-alone diagnosis (although some experts disagree), and the term is used to describe a feature of the underlying disorder.
Recognising and treating catatonia is very important as failure to do this can lead to poor outcomes and can be potentially fatal. Treatment with benzodiazepines or ECT can lead to remission of catatonia. There is growing evidence of the effectiveness of the NMDA receptor antagonists amantadine and memantine for benzodiazepine-resistant catatonia. Antipsychotics are sometimes employed, but they can worsen symptoms and have serious adverse effects.
It was first described in 1874 by Karl Ludwig Kahlbaum as Die Katatonie oder das Spannungsirresein (Catatonia or Tension Insanity).
Catatonia is almost always secondary to another underlying illness, often a psychiatric disorder. Mood disorders such as a bipolar disorder and depression are the most common aetiologies to progress to catatonia. Other psychiatric associations include schizophrenia and other primary psychotic disorders. It also is related to autism spectrum disorders.
Catatonia is also seen in many medical disorders, including infections (such as encephalitis), autoimmune disorders, meningitis, focal neurological lesions (including strokes), alcohol withdrawal, abrupt or overly rapid benzodiazepine withdrawal, cerebrovascular disease, neoplasms, head injury, and some metabolic conditions (homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcaemia).
Catatonia has been mostly studied in acutely ill psychiatric patients. Catatonia frequently goes unrecognised, leading to the belief that the syndrome is rare, however, this is not true and prevalence has been reported to be as high as 10% in patients with acute psychiatric illnesses. 21-46% of all catatonia cases can be attributed to a general medical condition.
The pathophysiology that leads to catatonia is still poorly understood and a definite mechanism remains unknown. Neurologic studies have implicated several pathways, however, it remains unclear whether these findings are the cause or the consequence of the disorder.
Abnormalities in GABA, glutamate signalling, serotonin, and dopamine transmission are believed to be implicated in catatonia.
Furthermore, it has also been hypothesized that pathways that connect the basal ganglia with the cortex and thalamus is involved in the development of catatonia.
Signs and Symptoms
The presentation of a patient with catatonia varies greatly depending on the subtype, underlying cause and it can be acute or subtle.
Because most patients with catatonia have an underlying psychiatric illness, the majority will present with worsening depression, mania, or psychosis followed by catatonia symptoms. Catatonia presents as a motor disturbance in which patients will display marked reduction in movement, marked agitation, or a mixture of both despite having the physical capacity to move normally. These patients may be unable to start an action or stop one. Movements and mannerisms may be repetitive, or purposeless.
The most common signs of catatonia are immobility, mutism, withdrawal and refusal to eat, staring, negativism, posturing (rigidity), rigidity, waxy flexibility/catalepsy, stereotypy (purposeless, repetitive movements), echolalia or echopraxia, verbigeration (repeat meaningless phrases). It should not be assumed that patients presenting with catatonia are unaware of their surroundings as some patients can recall in detail their catatonic state and their actions.
There are several subtypes of catatonia and they are characterised by the specific movement disturbance and associated features. Although catatonia can be divided into various subtypes, the natural history of catatonia is often fluctuant and different states can exist within the same individual.
This form of catatonia is characterised by decreased response to external stimuli, immobility or inhibited movement, mutism, staring, posturing, and negativism.
Patients may sit or stand in the same position for hours, may hold odd positions, and may resist movement of their extremities.
Excited catatonia is characterised by odd mannerisms/gestures, performing purposeless or inappropriate actions, excessive motor activity restlessness, stereotypy, impulsivity, agitation, combativeness.
Speech and actions may be repetitive or mimic another person’s.
People in this state are extremely hyperactive and may have delusions and hallucinations.
Catatonic excitement is commonly cited as one of the most dangerous mental states in psychiatry.
Malignant catatonia is a life-threatening condition that may progress rapidly within a few days. It is characterised by fever, abnormalities in blood pressure, heart rate, respiratory rate, diaphoresis (sweating), and delirium.
Certain lab findings are common with this presentation, however, they are nonspecific which means that they are also present in other conditions and do not diagnose catatonia.
The signs and symptoms of malignant catatonia overlap significantly with neuroleptic malignant syndrome (NMS) and so a careful history, review of medications, and physical exam are critical to properly differentiate these conditions.
For example, if the patient has waxy flexibility and holds a position against gravity when passively moved into that position, then it is likely catatonia.
If the patient has a “lead-pipe rigidity” then NMS should be the prime suspect.
There is not yet a definitive consensus regarding diagnostic criteria of catatonia. In the American Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the World Health Organisation’s eleventh edition of the International Classification of Disease (ICD-11) the classification is more homogeneous than in earlier editions. Prominent researchers in the field have other suggestions for diagnostic criteria.
The DSM-5 does not classify catatonia as an independent disorder, but rather it classifies it as catatonia associated with another mental disorder, due to another medical condition, or as unspecified catatonia. Catatonia is diagnosed by the presence of three or more of the following 12 psychomotor symptoms in association with the above mentioned mental disorder, medical condition, or unspecified.
Stupor: no psycho-motor activity; not actively relating to environment.
Catalepsy: passive induction of a posture held against gravity.
Waxy flexibility: allowing positioning by examiner and maintaining that position.
Mutism: no, or very little, verbal response (exclude if known aphasia).
Negativism: opposition or no response to instructions or external stimuli.
Posturing: spontaneous and active maintenance of a posture against gravity.
Mannerisms that are odd, circumstantial caricatures of normal actions.
Other disorders (additional code 293.89 [F06.1] to indicate the presence of the co-morbid catatonia):
Catatonia associated with autism spectrum disorder.
Catatonia associated with schizophrenia spectrum and other psychotic disorders.
Catatonia associated with brief psychotic disorder.
Catatonia associated with schizophreniform disorder.
Catatonia associated with schizoaffective disorder.
Catatonia associated with substance-induced psychotic disorder.
Catatonia associated with bipolar and related disorders.
Catatonia associated with major depressive disorder.
Catatonic disorder due to another medical condition.
If catatonic symptoms are present but do not form the catatonic syndrome, a medication- or substance-induced aetiology should first be considered.
In ICD-11 catatonia is defined as a syndrome of primarily psychomotor disturbances that is characterised by the simultaneous occurrence of several symptoms such as stupor; catalepsy; waxy flexibility; mutism; negativism; posturing; mannerisms; stereotypies; psychomotor agitation; grimacing; echolalia and echopraxia. Catatonia may occur in the context of specific mental disorders, including mood disorders, schizophrenia or other primary psychotic disorders, and Neurodevelopmental disorders, and may be induced by psychoactive substances, including medications. Catatonia may also be caused by a medical condition not classified under mental, behavioural, or neurodevelopmental disorders.
Catatonia is often overlooked and under-diagnosed. Patients with catatonia most commonly have an underlying psychiatric disorder, for this reason, physicians may overlook signs of catatonia due to the severity of the psychosis the patient is presenting with. Furthermore, the patient may not be presenting with the common signs of catatonia such as mutism and posturing. Additionally, the motor abnormalities seen in catatonia are also present in psychiatric disorders. For example, a patient with mania will show increased motor activity that may progress to excited catatonia. One way in which physicians can differentiate between the two is to observe the motor abnormality. Patients with mania present with increased goal-directed activity. On the other hand, the increased activity in catatonia is not goal-directed and often repetitive.
Catatonia is a clinical diagnosis and there is no specific laboratory test to diagnose it. However, certain testing can help determine what is causing the catatonia. An EEG will likely show diffuse slowing. If a seizure activity is driving the syndrome, then an EEG would also be helpful in detecting this. CT or MRI will not show catatonia; however, they might reveal abnormalities that might be leading to the syndrome. Metabolic screens, inflammatory markers, or autoantibodies may reveal reversible medical causes of catatonia.
Vital signs should be frequently monitored as catatonia can progress to malignant catatonia which is life-threatening. Malignant catatonia is characterised by fever, hypertension, tachycardia, and tachypnoea.
Various rating scales for catatonia have been developed, however, their utility for clinical care has not been well established. The most commonly used scale is the Bush-Francis Catatonia Rating Scale (BFCRS) (downloadable PDF). The scale is composed of 23 items with the first 14 items being used as the screening tool. If 2 of the 14 are positive, this prompts for further evaluation and completion of the remaining 9 items.
A diagnosis can be supported by the lorazepam challenge or the zolpidem challenge. While proven useful in the past, barbiturates are no longer commonly used in psychiatry; thus the option of either benzodiazepines or ECT.
The differential diagnosis of catatonia is extensive as signs and symptoms of catatonia may overlap significantly with those of other conditions. Therefore, a careful and detailed history, medication review, and physical exam are key to diagnosing catatonia and differentiating it from other conditions. Furthermore, some of these conditions can themselves lead to catatonia. The differential diagnosis is as follows:
Neuroleptic malignant syndrome (NMS):
Malignant catatonia and NMS are both life-threatening conditions that share many of the same characteristics including fever, autonomic instability, rigidity, and delirium.
Lab values of low serum iron, elevated creatine kinase, and white blood cell count are also shared by the two disorders further complicating the diagnosis.
Some experts consider NMS a drug-induced form of catatonia, however, it has not been established as a subtype.
There are features of malignant catatonia (posturing, impulsivity, etc) that are absent from NSM and the lab results are not as consistent in malignant catatonia as they are in NMS.
NMS is a drug-induced condition associated with antipsychotics, particularly, first generation antipsychotics.
Therefore, discontinuing antipsychotics and starting benzodiazepines is a treatment for this condition, and similarly it is helpful in catatonia as well.
Anti-NMDA receptor encephalitis:
Anti-NMDA receptor encephalitis is an autoimmune disorder characterised by neuropsychiatric features and the presence of IgG antibodies.
The presentation of anti-NMDAR encephalitis has been categorized into 5 phases: prodromal phase, psychotic phase, unresponsive phase, hyperkinetic phase, and recovery phase.
The psychotic phase progresses into the unresponsive phase characterized by mutism, decreased motor activity, and catatonia.
Both serotonin syndrome and malignant catatonia may present with signs and symptoms of delirium, autonomic instability, hyperthermia, and rigidity.
Again, similar to the presentation in NSM. However, patients with Serotonin syndrome have a history of ingestion of serotonergic drugs (Ex: SSRI).
These patients will also present with hyperreflexia, myoclonus, nausea, vomiting, and diarrhoea.
Malignant hyperthermia and malignant catatonia share features of autonomic instability, hyperthermia, and rigidity.
However, malignant hyperthermia is a hereditary disorder of skeletal muscle that makes these patients susceptible to exposure to halogenated anaesthetics and/or depolarising muscle relaxants like succinylcholine.
Malignant hyperthermia most commonly occurs in the intraoperative or postoperative periods. Other signs and symptoms of malignant hyperthermia include metabolic and respiratory acidosis, hyperkalaemia, and cardiac arrhythmias.
Akinetic mutism is a neurological disorder characterised by a decrease in goal-directed behaviour and motivation, however, the patient has an intact level of consciousness.
Patients may present with apathy, and may seem indifferent to pain, hunger, or thirst.
Akinetic mutism has been associated with structural damage in a variety of brain areas.
Akinetic mutism and catatonia may both manifest with immobility, mutism, and waxy flexibility.
Differentiating both disorders is the fact that akinetic mutism does not present with echolalia, echopraxia, or posturing.
Furthermore, it is not responsive to benzodiazepines as is the case for catatonia.
Elective mutism has an anxious aetiology but has also been associated with personality disorders.
Patients with this disorder fail to speak with some individuals but will speak with others.
Likewise, they may refuse to speak in certain situations, for example, a child who refuses to speak at school but is conversational at home.
This disorder is distinguished from catatonia by the absence of any other signs/symptoms.
Non-convulsive status epilepticus:
Non-convulsive status epilepticus is seizure activity with no accompanying tonic-clonic movements.
It can present with stupor, similar to catatonia, and they both respond to benzodiazepines.
Non-convulsive status epilepticus is diagnosed by the presence of seizure activity seen on electroencephalogram (EEG).
Catatonia on the other hand, is associated with normal EEG or diffuse slowing.
Delirium is characterised by fluctuating disturbed perception and consciousness in the ill individual.
It has hypoactive and hyperactive or mixed forms. People with hyperactive delirium present similarly to those with excited catatonia and have symptoms of restlessness, agitation and aggression.
Those with hypoactive delirium present with similarly to retarded catatonia, withdrawn and quiet.
However, catatonia also includes other distinguishing features including posturing and rigidity as well as a positive response to benzodiazepines.
Patients with locked-in syndrome present with immobility and mutism, however, unlike patients with catatonia who are unmotivated to communicate, patients with locked-in syndrome try to communicate with eye movements and blinking.
Furthermore, locked-in syndrome is caused by damage to the brainstem.
Catatonia and stiff-person syndrome are similar in that they may both present with rigidity, autonomic instability and a positive response to benzodiazepines.
However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies and other catatonic signs such as mutism and posturing are not part of the syndrome.
Untreated late-stage Parkinson’s disease may present similarly to retarded catatonia with symptoms of immobility, rigidity, and difficulty speaking.
Further complicating the diagnosis is the fact that many patients with Parkinson’s disease will have major depressive disorder which may be the underlying cause of catatonia.
Parkinson’s disease can be distinguished from catatonia by a positive response to levodopa.
Catatonia on the other hand will show a positive response to benzodiazepines.
The initial treatment of catatonia is to stop medication that could be potentially leading to the syndrome. These may include steroids, stimulants, anticonvulsants, neuroleptics, dopamine blockers, etc. The next step is to provide a “lorazepam challenge,” in which patients are given 2 mg of IV lorazepam (or another benzodiazepine). Most patients with catatonia will respond significantly to this within the first 15-30 minutes. If no change is observed during the first dose, then a second dose is given and the patient is re-examined. If the patient responds to the lorazepam challenge, then lorazepam can be scheduled at interval doses until the catatonia resolves. The lorazepam must be tapered slowly, otherwise, the catatonia symptoms may return. The underlying cause of the catatonia should also be treated during this time. If within a week the catatonia is not resolved, then ECT can be used to reverse the symptoms. ECT in combination with benzodiazepines is used to treat malignant catatonia. In France, zolpidem has also been used in diagnosis, and response may occur within the same time period. Ultimately the underlying cause needs to be treated.
Electroconvulsive therapy (ECT) is an effective treatment for catatonia that is well acknowledged. ECT has also shown favourable outcomes in patients with chronic catatonia. However, it has been pointed out that further high quality randomised controlled trials are needed to evaluate the efficacy, tolerance, and protocols of ECT in catatonia.
Antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic.
Excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, NMDA antagonists such as amantadine or memantine may be used. Amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. Memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. Topiramate is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of AMPA receptors.
Complications, Outcomes, and Recurrence
Patients may suffer several complications from being in a catatonic state. The nature of these complications will depend on the type of catatonia being experienced by the patient. For example, patients presenting with retarded catatonia may have refusal to eat which will in turn lead to malnutrition and dehydration. Furthermore, if immobility is a symptom the patient is presenting with, then they may develop pressure ulcers, muscle contractions, and are at risk of developing deep vein thrombosis (DVT) and pulmonary embolus (PE). Patients with excited catatonia may be aggressive and violent, and physical trauma may result from this. Catatonia may progress to the malignant type which will present with autonomic instability and may be life threatening. Other complications also include the development of pneumonia and neuroleptic malignant syndrome.
Patients who experience an episode of catatonia are more likely to suffer recurrence. Treatment response for patients with catatonia is 50-70% and these patients have a good prognosis. However, failure to respond to medication is a very poor prognosis. Many of these patients will require long-term and continuous mental health care. For patients with catatonia with underlying schizophrenia, the prognosis is much poorer.
Into the Abyss: A Neuropsychiatrist’s Notes on Troubled Minds.
Author(s): Anthony David.
Edition: First (1st), Reprint Edition.
Publisher: Oneworld Publications.
Type(s): Paperback, Audiobook, and Kindle.
We cannot know how to fix a problem until we understand its causes. But even for some of the most common mental health problems, specialists argue over whether the answers lie in the person’s biology, their psychology or their circumstances.
As a cognitive neuropsychiatrist, Anthony David brings together many fields of enquiry, from social and cognitive psychology to neurology. The key for each patient might be anything from a traumatic memory to a chemical imbalance, an unhealthy way of thinking or a hidden tumour.
Patrick believes he is dead. Jennifer’s schizophrenia medication helped with her voices but did it cause Parkinson’s? Emma is in a coma – or is she just refusing to respond?
Drawing from Professor David’s career as a clinician and academic, these fascinating case studies reveal the unique complexity of the human mind, stretching the limits of our understanding.
Neuroscience (or neurobiology) is the scientific study of the nervous system. It is a multidisciplinary science that combines physiology, anatomy, molecular biology, developmental biology, cytology, mathematical modelling, and psychology to understand the fundamental and emergent properties of neurons and neural circuits. The understanding of the biological basis of learning, memory, behaviour, perception, and consciousness has been described by Eric Kandel as the “ultimate challenge” of the biological sciences.
The scope of neuroscience has broadened over time to include different approaches used to study the nervous system at different scales and the techniques used by neuroscientists have expanded enormously, from molecular and cellular studies of individual neurons to imaging of sensory, motor and cognitive tasks in the brain.
The earliest study of the nervous system dates to ancient Egypt. Trepanation, the surgical practice of either drilling or scraping a hole into the skull for the purpose of curing head injuries or mental disorders, or relieving cranial pressure, was first recorded during the Neolithic period. Manuscripts dating to 1700 BC indicate that the Egyptians had some knowledge about symptoms of brain damage.
Early views on the function of the brain regarded it to be a “cranial stuffing” of sorts. In Egypt, from the late Middle Kingdom onwards, the brain was regularly removed in preparation for mummification. It was believed at the time that the heart was the seat of intelligence. According to Herodotus, the first step of mummification was to “take a crooked piece of iron, and with it draw out the brain through the nostrils, thus getting rid of a portion, while the skull is cleared of the rest by rinsing with drugs.”
The view that the heart was the source of consciousness was not challenged until the time of the Greek physician Hippocrates. He believed that the brain was not only involved with sensation – since most specialised organs (e.g. eyes, ears, tongue) are located in the head near the brain – but was also the seat of intelligence. Plato also speculated that the brain was the seat of the rational part of the soul. Aristotle, however, believed the heart was the centre of intelligence and that the brain regulated the amount of heat from the heart. This view was generally accepted until the Roman physician Galen, a follower of Hippocrates and physician to Roman gladiators, observed that his patients lost their mental faculties when they had sustained damage to their brains.
Abulcasis, Averroes, Avicenna, Avenzoar, and Maimonides, active in the Medieval Muslim world, described a number of medical problems related to the brain. In Renaissance Europe, Vesalius (1514-1564), René Descartes (1596-1650), Thomas Willis (1621-1675) and Jan Swammerdam (1637-1680) also made several contributions to neuroscience.
Luigi Galvani’s pioneering work in the late 1700s set the stage for studying the electrical excitability of muscles and neurons. In the first half of the 19th century, Jean Pierre Flourens pioneered the experimental method of carrying out localised lesions of the brain in living animals describing their effects on motricity, sensibility and behaviour. In 1843 Emil du Bois-Reymond demonstrated the electrical nature of the nerve signal, whose speed Hermann von Helmholtz proceeded to measure, and in 1875 Richard Caton found electrical phenomena in the cerebral hemispheres of rabbits and monkeys. Adolf Beck published in 1890 similar observations of spontaneous electrical activity of the brain of rabbits and dogs. Studies of the brain became more sophisticated after the invention of the microscope and the development of a staining procedure by Camillo Golgi during the late 1890s. The procedure used a silver chromate salt to reveal the intricate structures of individual neurons. His technique was used by Santiago Ramón y Cajal and led to the formation of the neuron doctrine, the hypothesis that the functional unit of the brain is the neuron. Golgi and Ramón y Cajal shared the Nobel Prize in Physiology or Medicine in 1906 for their extensive observations, descriptions, and categorizations of neurons throughout the brain.
In parallel with this research, work with brain-damaged patients by Paul Broca suggested that certain regions of the brain were responsible for certain functions. At the time, Broca’s findings were seen as a confirmation of Franz Joseph Gall’s theory that language was localised and that certain psychological functions were localised in specific areas of the cerebral cortex. The localisation of function hypothesis was supported by observations of epileptic patients conducted by John Hughlings Jackson, who correctly inferred the organisation of the motor cortex by watching the progression of seizures through the body. Carl Wernicke further developed the theory of the specialisation of specific brain structures in language comprehension and production. Modern research through neuroimaging techniques, still uses the Brodmann cerebral cytoarchitectonic map (referring to study of cell structure) anatomical definitions from this era in continuing to show that distinct areas of the cortex are activated in the execution of specific tasks.
During the 20th century, neuroscience began to be recognised as a distinct academic discipline in its own right, rather than as studies of the nervous system within other disciplines. Eric Kandel and collaborators have cited David Rioch, Francis O. Schmitt, and Stephen Kuffler as having played critical roles in establishing the field. Rioch originated the integration of basic anatomical and physiological research with clinical psychiatry at the Walter Reed Army Institute of Research, starting in the 1950s. During the same period, Schmitt established a neuroscience research programme within the Biology Department at the Massachusetts Institute of Technology, bringing together biology, chemistry, physics, and mathematics. The first freestanding neuroscience department (then called Psychobiology) was founded in 1964 at the University of California, Irvine by James L. McGaugh. This was followed by the Department of Neurobiology at Harvard Medical School, which was founded in 1966 by Stephen Kuffler.
The understanding of neurons and of nervous system function became increasingly precise and molecular during the 20th century. For example, in 1952, Alan Lloyd Hodgkin and Andrew Huxley presented a mathematical model for transmission of electrical signals in neurons of the giant axon of a squid, which they called “action potentials”, and how they are initiated and propagated, known as the Hodgkin-Huxley model. In 1961–1962, Richard FitzHugh and J. Nagumo simplified Hodgkin-Huxley, in what is called the FitzHugh-Nagumo model. In 1962, Bernard Katz modelled neurotransmission across the space between neurons known as synapses. Beginning in 1966, Eric Kandel and collaborators examined biochemical changes in neurons associated with learning and memory storage in Aplysia. In 1981 Catherine Morris and Harold Lecar combined these models in the Morris-Lecar model. Such increasingly quantitative work gave rise to numerous biological neuron models and models of neural computation.
As a result of the increasing interest about the nervous system, several prominent neuroscience organizations have been formed to provide a forum to all neuroscientist during the 20th century. For example, the International Brain Research Organisation was founded in 1961, the International Society for Neurochemistry in 1963, the European Brain and Behaviour Society in 1968, and the Society for Neuroscience in 1969. Recently, the application of neuroscience research results has also given rise to applied disciplines as neuroeconomics, neuroeducation, neuroethics, and neurolaw.
Over time, brain research has gone through philosophical, experimental, and theoretical phases, with work on brain simulation predicted to be important in the future.
The scientific study of the nervous system increased significantly during the second half of the twentieth century, principally due to advances in molecular biology, electrophysiology, and computational neuroscience. This has allowed neuroscientists to study the nervous system in all its aspects: how it is structured, how it works, how it develops, how it malfunctions, and how it can be changed.
For example, it has become possible to understand, in much detail, the complex processes occurring within a single neuron. Neurons are cells specialised for communication. They are able to communicate with neurons and other cell types through specialised junctions called synapses, at which electrical or electrochemical signals can be transmitted from one cell to another. Many neurons extrude a long thin filament of axoplasm called an axon, which may extend to distant parts of the body and are capable of rapidly carrying electrical signals, influencing the activity of other neurons, muscles, or glands at their termination points. A nervous system emerges from the assemblage of neurons that are connected to each other.
The vertebrate nervous system can be split into two parts: the central nervous system (defined as the brain and spinal cord), and the peripheral nervous system. In many species – including all vertebrates – the nervous system is the most complex organ system in the body, with most of the complexity residing in the brain. The human brain alone contains around one hundred billion neurons and one hundred trillion synapses; it consists of thousands of distinguishable substructures, connected to each other in synaptic networks whose intricacies have only begun to be unravelled. At least one out of three of the approximately 20,000 genes belonging to the human genome is expressed mainly in the brain.
Due to the high degree of plasticity of the human brain, the structure of its synapses and their resulting functions change throughout life.
Making sense of the nervous system’s dynamic complexity is a formidable research challenge. Ultimately, neuroscientists would like to understand every aspect of the nervous system, including how it works, how it develops, how it malfunctions, and how it can be altered or repaired. Analysis of the nervous system is therefore performed at multiple levels, ranging from the molecular and cellular levels to the systems and cognitive levels. The specific topics that form the main foci of research change over time, driven by an ever-expanding base of knowledge and the availability of increasingly sophisticated technical methods. Improvements in technology have been the primary drivers of progress. Developments in electron microscopy, computer science, electronics, functional neuroimaging, and genetics and genomics have all been major drivers of progress.
Molecular and Cellular Neuroscience
Basic questions addressed in molecular neuroscience include the mechanisms by which neurons express and respond to molecular signals and how axons form complex connectivity patterns. At this level, tools from molecular biology and genetics are used to understand how neurons develop and how genetic changes affect biological functions. The morphology, molecular identity, and physiological characteristics of neurons and how they relate to different types of behaviour are also of considerable interest.
Questions addressed in cellular neuroscience include the mechanisms of how neurons process signals physiologically and electrochemically. These questions include how signals are processed by neurites and somas and how neurotransmitters and electrical signals are used to process information in a neuron. Neurites are thin extensions from a neuronal cell body, consisting of dendrites (specialised to receive synaptic inputs from other neurons) and axons (specialised to conduct nerve impulses called action potentials). Somas are the cell bodies of the neurons and contain the nucleus.
Another major area of cellular neuroscience is the investigation of the development of the nervous system. Questions include the patterning and regionalisation of the nervous system, neural stem cells, differentiation of neurons and glia (neurogenesis and gliogenesis), neuronal migration, axonal and dendritic development, trophic interactions, and synapse formation.
Computational neurogenetic modelling is concerned with the development of dynamic neuronal models for modelling brain functions with respect to genes and dynamic interactions between genes.
Neural Circuits and Systems
Questions in systems neuroscience include how neural circuits are formed and used anatomically and physiologically to produce functions such as reflexes, multisensory integration, motor coordination, circadian rhythms, emotional responses, learning, and memory. In other words, they address how these neural circuits function in large-scale brain networks, and the mechanisms through which behaviours are generated. For example, systems level analysis addresses questions concerning specific sensory and motor modalities: how does vision work? How do songbirds learn new songs and bats localize with ultrasound? How does the somatosensory system process tactile information? The related fields of neuroethology and neuropsychology address the question of how neural substrates underlie specific animal and human behaviours. Neuroendocrinology and psychoneuroimmunology examine interactions between the nervous system and the endocrine and immune systems, respectively. Despite many advancements, the way that networks of neurons perform complex cognitive processes and behaviours is still poorly understood.
Cognitive and Behavioural Neuroscience
Cognitive neuroscience addresses the questions of how psychological functions are produced by neural circuitry. The emergence of powerful new measurement techniques such as neuroimaging (e.g. fMRI, PET, SPECT), EEG, MEG, electrophysiology, optogenetics and human genetic analysis combined with sophisticated experimental techniques from cognitive psychology allows neuroscientists and psychologists to address abstract questions such as how cognition and emotion are mapped to specific neural substrates. Although many studies still hold a reductionist stance looking for the neurobiological basis of cognitive phenomena, recent research shows that there is an interesting interplay between neuroscientific findings and conceptual research, soliciting and integrating both perspectives. For example, neuroscience research on empathy solicited an interesting interdisciplinary debate involving philosophy, psychology and psychopathology. Moreover, the neuroscientific identification of multiple memory systems related to different brain areas has challenged the idea of memory as a literal reproduction of the past, supporting a view of memory as a generative, constructive and dynamic process.
Neuroscience is also allied with the social and behavioural sciences as well as nascent interdisciplinary fields such as neuroeconomics, decision theory, social neuroscience, and neuromarketing to address complex questions about interactions of the brain with its environment. A study into consumer responses for example uses EEG to investigate neural correlates associated with narrative transportation into stories about energy efficiency.
Questions in computational neuroscience can span a wide range of levels of traditional analysis, such as development, structure, and cognitive functions of the brain. Research in this field utilises mathematical models, theoretical analysis, and computer simulation to describe and verify biologically plausible neurons and nervous systems. For example, biological neuron models are mathematical descriptions of spiking neurons which can be used to describe both the behaviour of single neurons as well as the dynamics of neural networks. Computational neuroscience is often referred to as theoretical neuroscience.
Nanoparticles in medicine are versatile in treating neurological disorders showing promising results in mediating drug transport across the blood brain barrier. Implementing nanoparticles in antiepileptic drugs enhances their medical efficacy by increasing bioavailability in the bloodstream, as well as offering a measure of control in release time concentration. Although nanoparticles can assist therapeutic drugs by adjusting physical properties to achieve desirable effects, inadvertent increases in toxicity often occur in preliminary drug trials. Furthermore, production of nanomedicine for drug trials is economically consuming, hindering progress in their implementation. Computational models in nanoneuroscience provide alternatives to study the efficacy of nanotechnology-based medicines in neurological disorders while mitigating potential side effects and development costs.
Nanomaterials often operate at length scales between classical and quantum regimes. Due to the associated uncertainties at the length scales that nanomaterials operate, it is difficult to predict their behaviour prior to in vivo studies. Classically, the physical processes which occur throughout neurons are analogous to electrical circuits. Designers focus on such analogies and model brain activity as a neural circuit. Success in computational modelling of neurons have led to the development of stereochemical models that accurately predict acetylcholine receptor-based synapses operating at microsecond time scales.
Ultrafine nanoneedles for cellular manipulations are thinner than the smallest single walled carbon nanotubes. Computational quantum chemistry is used to design ultrafine nanomaterials with highly symmetrical structures to optimise geometry, reactivity and stability.
Behaviour of nanomaterials are dominated by long ranged non-bonding interactions. Electrochemical processes that occur throughout the brain generate an electric field which can inadvertently affect the behaviour of some nanomaterials. Molecular dynamics simulations can mitigate the development phase of nanomaterials as well as prevent neural toxicity of nanomaterials following in vivo clinical trials. Testing nanomaterials using molecular dynamics optimizes nano characteristics for therapeutic purposes by testing different environment conditions, nanomaterial shape fabrications, nanomaterial surface properties, etc without the need for in vivo experimentation. Flexibility in molecular dynamic simulations allows medical practitioners to personalise treatment. Nanoparticle related data from translational nanoinformatics links neurological patient specific data to predict treatment response.
The visualization of neuronal activity is of key importance in the study of neurology. Nano-imaging tools with nanoscale resolution help in these areas. These optical imaging tools are PALM and STORM which helps visualise nanoscale objects within cells. Pampaloni states that, so far, these imaging tools revealed the dynamic behaviour and organisation of the actin cytoskeleton inside the cells, which will assist in understanding how neurons probe their involvement during neuronal outgrowth and in response to injury, and how they differentiate axonal processes and characterisation of receptor clustering and stoichiometry at the plasma inside the synapses, which are critical for understanding how synapses respond to changes in neuronal activity. These past works focused on devices for stimulation or inhibition of neural activity, but the crucial aspect is the ability for the device to simultaneously monitor neural activity. The major aspect that is to be improved in the nano imaging tools is the effective collection of the light as a major problem is that biological tissue are dispersive media that do not allow a straightforward propagation and control of light. These devices use nanoneedle and nanowire (NWs) for probing and stimulation.
NWs are artificial nano- or micro-sized “needles” that can provide high-fidelity electrophysiological recordings if used as microscopic electrodes for neuronal recordings. NWs are an attractive as they are highly functional structures that offer unique electronic properties that are affected by biological/chemical species adsorbed on their surface; mostly the conductivity. This conductivity variance depending on chemical species present allows enhanced sensing performances. NWs are also able to act as non-invasive and highly local probes. These versatility of NWs makes it optimal for interfacing with neurons due to the fact that the contact length along the axon (or the dendrite projection crossing a NW) is just about 20 nm.
Neuroscience and Medicine
Neurology, psychiatry, neurosurgery, psychosurgery, anesthesiology and pain medicine, neuropathology, neuroradiology, ophthalmology, otolaryngology, clinical neurophysiology, addiction medicine, and sleep medicine are some medical specialties that specifically address the diseases of the nervous system. These terms also refer to clinical disciplines involving diagnosis and treatment of these diseases.
Neurology works with diseases of the central and peripheral nervous systems, such as amyotrophic lateral sclerosis (ALS) and stroke, and their medical treatment. Psychiatry focuses on affective, behavioural, cognitive, and perceptual disorders. Anaesthesiology focuses on perception of pain, and pharmacologic alteration of consciousness. Neuropathology focuses upon the classification and underlying pathogenic mechanisms of central and peripheral nervous system and muscle diseases, with an emphasis on morphologic, microscopic, and chemically observable alterations. Neurosurgery and psychosurgery work primarily with surgical treatment of diseases of the central and peripheral nervous systems.
Recently, the boundaries between various specialties have blurred, as they are all influenced by basic research in neuroscience. For example, brain imaging enables objective biological insight into mental illnesses, which can lead to faster diagnosis, more accurate prognosis, and improved monitoring of patient progress over time.
Integrative neuroscience describes the effort to combine models and information from multiple levels of research to develop a coherent model of the nervous system. For example, brain imaging coupled with physiological numerical models and theories of fundamental mechanisms may shed light on psychiatric disorders.
One of the main goals of nanoneuroscience is to gain a detailed understanding of how the nervous system operates and, thus, how neurons organise themselves in the brain. Consequently, creating drugs and devices that are able to cross the blood brain barrier (BBB) are essential to allow for detailed imaging and diagnoses. The blood brain barrier functions as a highly specialised semipermeable membrane surrounding the brain, preventing harmful molecules that may be dissolved in the circulation blood from entering the central nervous system.
The main two hurdles for drug-delivering molecules to access the brain are size (must have a molecular weight < 400 Da) and lipid solubility. Physicians hope to circumvent difficulties in accessing the central nervous system through viral gene therapy. This often involves direct injection into the patient’s brain or cerebral spinal fluid. The drawback of this therapy is that it is invasive and carries a high risk factor due to the necessity of surgery for the treatment to be administered. Because of this, only 3.6% of clinical trials in this field have progressed to stage III since the concept of gene therapy was developed in the 1980s.
Another proposed way to cross the BBB is through temporary intentional disruption of the barrier. This method was first inspired by certain pathological conditions that were discovered to break down this barrier by themselves, such as Alzheimer’s disease, Parkinson’s disease, stroke, and seizure conditions.
Nanoparticles are unique from macromolecules because their surface properties are dependent on their size, allowing for strategic manipulation of these properties (or, “programming”) by scientists that would not be possible otherwise. Likewise, nanoparticle shape can also be varied to give a different set of characteristics based on the surface area to volume ratio of the particle.
Nanoparticles have promising therapeutic effects when treating neurodegenerative diseases. Oxygen reactive polymer (ORP) is a nano-platform programmed to react with oxygen and has been shown to detect and reduce the presence of reactive oxygen species (ROS) formed immediately after traumatic brain injuries. Nanoparticles have also been employed as a “neuroprotective” measure, as is the case with Alzheimer’s disease and stroke models. Alzheimer’s disease results in toxic aggregates of the amyloid beta protein formed in the brain. In one study, gold nanoparticles were programmed to attach themselves to these aggregates and were successful in breaking them up. Likewise, with ischemic stroke models, cells in the affected region of the brain undergo apoptosis, dramatically reducing blood flow to important parts of the brain and often resulting in death or severe mental and physical changes. Platinum nanoparticles have been shown to act as ROS, serving as “biological antioxidants” and significantly reducing oxidation in the brain as a result of stroke. Nanoparticles can also lead to neurotoxicity and cause permanent BBB damage either from brain oedema or from unrelated molecules crossing the BBB and causing brain damage. This proves further long term in vivo studies are needed to gain enough understanding to allow for successful clinical trials.
One of the most common nano-based drug delivery platforms is liposome-based delivery. They are both lipid-soluble and nano-scale and thus are permitted through a fully functioning BBB. Additionally, lipids themselves are biological molecules, making them highly biocompatible, which in turn lowers the risk of cell toxicity. The bilayer that is formed allows the molecule to fully encapsulate any drug, protecting it while it is travelling through the body. One drawback to shielding the drug from the outside cells is that it no longer has specificity, and requires coupling to extra antibodies to be able to target a biological site. Due to their low stability, liposome-based nanoparticles for drug delivery have a short shelf life.
Targeted therapy using magnetic nanoparticles (MNPs) is also a popular topic of research and has led to several stage III clinical trials. Invasiveness is not an issue here because a magnetic force can be applied from the outside of a patient’s body to interact and direct the MNPs. This strategy has been proven successful in delivering Brain-derived neurotropic factor, a naturally occurring gene thought to promote neurorehabilitation, across the BBB.
Modern neuroscience education and research activities can be very roughly categorised into the following major branches, based on the subject and scale of the system in examination as well as distinct experimental or curricular approaches. Individual neuroscientists, however, often work on questions that span several distinct subfields.
Affective neuroscience is the study of the neural mechanisms involved in emotion, typically through experimentation on animal models.
Behavioural neuroscience (also known as biological psychology, physiological psychology, biopsychology, or psychobiology) is the application of the principles of biology to the study of genetic, physiological, and developmental mechanisms of behaviour in humans and non-human animals.
Cellular neuroscience is the study of neurons at a cellular level including morphology and physiological properties.
The scientific study of the biological mechanisms that underlie the disorders and diseases of the nervous system.
Cognitive neuroscience is the study of the biological mechanisms underlying cognition.
Computational neuroscience is the theoretical study of the nervous system.
Cultural neuroscience is the study of how cultural values, practices and beliefs shape and are shaped by the mind, brain and genes across multiple timescales.
Developmental neuroscience studies the processes that generate, shape, and reshape the nervous system and seeks to describe the cellular basis of neural development to address underlying mechanisms.
Evolutionary neuroscience studies the evolution of nervous systems.
Molecular neuroscience studies the nervous system with molecular biology, molecular genetics, protein chemistry, and related methodologies.
Neural engineering uses engineering techniques to interact with, understand, repair, replace, or enhance neural systems.
Neuroanatomy is the study of the anatomy of nervous systems.
Neurochemistry is the study of how neurochemicals interact and influence the function of neurons.
Neuroethology is the study of the neural basis of non-human animals behaviour.
Neurogastronomy is the study of flavour and how it affects sensation, cognition, and memory.
Neurogenetics is the study of the genetical basis of the development and function of the nervous system.
Neuroimaging includes the use of various techniques to either directly or indirectly image the structure and function of the brain.
Neuroimmunology is concerned with the interactions between the nervous and the immune system.
Neuroinformatics is a discipline within bioinformatics that conducts the organisation of neuroscience data and application of computational models and analytical tools.
Neurolinguistics is the study of the neural mechanisms in the human brain that control the comprehension, production, and acquisition of language.
Neurophysics deals with the development of physical experimental tools to gain information about the brain.
Neurophysiology is the study of the functioning of the nervous system, generally using physiological techniques that include measurement and stimulation with electrodes or optically with ion- or voltage-sensitive dyes or light-sensitive channels.
Neuropsychology is a discipline that resides under the umbrellas of both psychology and neuroscience, and is involved in activities in the arenas of both basic science and applied science. In psychology, it is most closely associated with biopsychology, clinical psychology, cognitive psychology, and developmental psychology. In neuroscience, it is most closely associated with the cognitive, behavioural, social, and affective neuroscience areas. In the applied and medical domain, it is related to neurology and psychiatry.
Paleoneurobiology is a field which combines techniques used in palaeontology and archaeology to study brain evolution, especially that of the human brain.
Social neuroscience is an interdisciplinary field devoted to understanding how biological systems implement social processes and behaviour, and to using biological concepts and methods to inform and refine theories of social processes and behaviour.
Systems neuroscience is the study of the function of neural circuits and systems.
The largest professional neuroscience organisation is the Society for Neuroscience (SFN), which is based in the United States but includes many members from other countries. Since its founding in 1969 the SFN has grown steadily: as of 2010 it recorded 40,290 members from 83 different countries. Annual meetings, held each year in a different American city, draw attendance from researchers, postdoctoral fellows, graduate students, and undergraduates, as well as educational institutions, funding agencies, publishers, and hundreds of businesses that supply products used in research.
Other major organisations devoted to neuroscience include the International Brain Research Organisation (IBRO), which holds its meetings in a country from a different part of the world each year, and the Federation of European Neuroscience Societies (FENS), which holds a meeting in a different European city every two years. FENS comprises a set of 32 national-level organisations, including the British Neuroscience Association, the German Neuroscience Society (Neurowissenschaftliche Gesellschaft), and the French Société des Neurosciences. The first National Honour Society in Neuroscience, Nu Rho Psi, was founded in 2006. Numerous youth neuroscience societies which support undergraduates, graduates and early career researchers also exist, like Project Encephalon.
In 2013, the BRAIN Initiative was announced in the US. An International Brain Initiative was created in 2017, currently integrated by more than seven national-level brain research initiatives (US, Europe, Allen Institute, Japan, China, Australia, Canada, Korea, Israel) spanning four continents.
Public Education and Outreach
In addition to conducting traditional research in laboratory settings, neuroscientists have also been involved in the promotion of awareness and knowledge about the nervous system among the general public and government officials. Such promotions have been done by both individual neuroscientists and large organisations. For example, individual neuroscientists have promoted neuroscience education among young students by organising the International Brain Bee, which is an academic competition for high school or secondary school students worldwide. In the United States, large organisations such as the Society for Neuroscience have promoted neuroscience education by developing a primer called Brain Facts, collaborating with public school teachers to develop Neuroscience Core Concepts for K-12 teachers and students, and cosponsoring a campaign with the Dana Foundation called Brain Awareness Week to increase public awareness about the progress and benefits of brain research. In Canada, the CIHR Canadian National Brain Bee is held annually at McMaster University.
Neuroscience educators formed Faculty for Undergraduate Neuroscience (FUN) in 1992 to share best practices and provide travel awards for undergraduates presenting at Society for Neuroscience meetings.
Finally, neuroscientists have also collaborated with other education experts to study and refine educational techniques to optimise learning among students, an emerging field called educational neuroscience. Federal agencies in the United States, such as the National Institute of Health (NIH) and National Science Foundation (NSF), have also funded research that pertains to best practices in teaching and learning of neuroscience concepts.
1895 – Walter Jackson Freeman II, American physician and psychiatrist (d. 1972).
2008 – Robert E. Valett, American psychologist, teacher, and author (b. 1927).
Walter Jackson Freeman II
Walter Jackson Freeman II (14 November 1895 to 31 May 1972) was an American physician who specialized in lobotomy.
Biography and Early Years
Walter J. Freeman was born on 14 November 1895, and raised in Philadelphia, Pennsylvania, by his parents. Freeman’s grandfather, William Williams Keen, was well known as a surgeon in the Civil War. His father was also a very successful doctor. Freeman attended Yale University beginning in 1912, and graduated in 1916. He then moved on to study neurology at the University of Pennsylvania Medical School. While attending medical school, he studied the work of William Spiller and idolized his groundbreaking work in the new field of the neurological sciences. Spiller also worked in Philadelphia and was credited by many in the world of psychology as being the founder of neurology. Freeman applied for a coveted position working alongside Spiller in his home town of Philadelphia, but was rejected.
Shortly afterward, in 1924, Freeman relocated to Washington, D.C., and started practicing as the first neurologist in the city. Upon his arrival in Washington, Freeman began work directing laboratories at St. Elizabeth’s Hospital. Working at the hospital and witnessing the pain and distress suffered by the patients encouraged him to continue his education in the field. Freeman earned his PhD in neuropathology within the following few years and secured a position at George Washington University in Washington, D.C., as head of the neurology department.
In 1932, his mother died at the Philadelphia Orthopaedic Hospital in Philadelphia, Pennsylvania.
The first systematic attempt at human psychosurgery – performed in the 1880s-1890s – is commonly attributed to the Swiss psychiatrist Gottlieb Burckhardt. Burckhardt’s experimental surgical forays were largely condemned at the time and in the subsequent decades psychosurgery was attempted only intermittently. On 12 November 1935, a new psychosurgery procedure was performed in Portugal under the direction of the neurologist and physician Egas Moniz. His new “leucotomy” procedure, intended to treat mental illness, took small corings of the patient’s frontal lobes. Moniz became a mentor and idol for Freeman who modified the procedure and renamed it the “lobotomy”. Instead of taking coring’s from the frontal lobes, Freeman’s procedure severed the connection between the frontal lobes and the thalamus. Because Freeman lost his license to perform surgery himself after his last patient died on the operating table, he enlisted neurosurgeon James Watts as a research partner. One year after the first leucotomy, on 14 September 1936, Freeman directed Watts through the very first prefrontal lobotomy in the United States on housewife Alice Hood Hammatt of Topeka, Kansas. By November, only two months after performing their first lobotomy surgery, Freeman and Watts had already worked on 20 cases including several follow-up operations. By 1942, the duo had performed over 200 lobotomy procedures and had published results claiming 63% of patients had improved, 24% were reported to be unchanged and 14% were worse after surgery.
After almost ten years of performing lobotomies, Freeman heard of a doctor in Italy named Amarro Fiamberti who operated on the brain through his patients’ eye sockets, allowing him to access the brain without drilling through the skull. After experimenting with novel ways of performing these brain surgeries, Freeman formulated a new procedure called the transorbital lobotomy. This new procedure became known as the “icepick” lobotomy and was performed by inserting a metal pick into the corner of each eye-socket, hammering it through the thin bone there with a mallet, and moving it back and forth, severing the connections to the prefrontal cortex in the frontal lobes of the brain. He performed the transorbital lobotomy surgery for the first time in Washington, D.C., on a housewife named Sallie Ellen Ionesco. This transorbital lobotomy method did not require a neurosurgeon and could be performed outside of an operating room without the use of anaesthesia by using electroconvulsive therapy to induce seizure. The modifications to his lobotomy allowed Freeman to broaden the use of the surgery, which could be performed in psychiatric hospitals throughout the United States that were overpopulated and understaffed. In 1950, Walter Freeman’s long-time partner James Watts left their practice and split from Freeman due to his opposition to the cruelty and overuse of the transorbital lobotomy.
Following his development of the transorbital lobotomy, Freeman travelled across the country visiting mental institutions, performing lobotomies and spreading his views and methods to institution staff (Contrary to myth, there is no evidence that he referred to the van that he travelled in as a “lobotomobile”). Freeman’s name gained popularity despite the widespread criticism of his methods following a lobotomy on President John F. Kennedy’s sister Rosemary Kennedy, which left her with severe mental and physical disability. A memoir written by former patient Howard Dully, called My Lobotomy documented his experiences with Freeman and his long recovery after undergoing a lobotomy surgery at 12 years of age. Walter Freeman charged just $25 for each procedure that he performed. After four decades Freeman had personally performed possibly as many as 4,000 lobotomy surgeries in 23 states, of which 2,500 used his ice-pick procedure, despite the fact that he had no formal surgical training. In February 1967, Freeman performed his final surgery on Helen Mortensen. Mortensen was a long-term patient and was receiving her third lobotomy from Freeman. She died of a cerebral haemorrhage, as did as many as 100 of his other patients, and he was finally banned from performing surgery. His patients often had to be retaught how to eat and use the bathroom. Relapses were common, some never recovered, and about 15% died from the procedure. In 1951, one patient at Iowa’s Cherokee Mental Health Institute died when Freeman suddenly stopped for a photo during the procedure, and the surgical instrument accidentally penetrated too far into the patient’s brain. Freeman wore neither gloves nor mask during these procedures. He lobotomised nineteen minors, including a four-year-old child.
At fifty-seven years old, Freeman retired from his position at George Washington University and opened up a modest practice in California.
An extensive collection of Freeman’s papers were donated to The George Washington University in 1980. The collection largely deals with the work that Freeman and James W. Watts did on psychosurgery over the course of their medical careers. The collection is currently under the care of GWU’s Special Collections Research Centre, located in the Estelle and Melvin Gelman Library.
Freeman was known for his eccentricities and he complemented his theatrical approach to demonstrating surgery by sporting a cane, goatee, and a narrow-brimmed hat.
Freeman died, of complications arising from an operation for cancer, on 31 May 1972.
He was survived by four children – Walter, Frank, Paul and Lorne – who became defenders of their father’s legacy. Paul became a psychiatrist in San Francisco and the eldest, Walter Jr., became a professor emeritus of neurobiology at University of California, Berkeley.
Contributions to Psychiatry
Walter Freeman nominated his mentor António Egas Moniz for a Nobel prize, and in 1949 Moniz won the Nobel prize in physiology and medicine. He pioneered and helped open up the psychiatric world to the idea of what would become psychosurgery. At the time, it was seen as a possible treatment for severe mental illness, but “within a few years, lobotomy was labelled one of the most barbaric mistakes of modern medicine.” He also helped to demonstrate the idea that mental events have a physiological basis. Despite his interest in the mind, Freeman was “uninterested in animal experiments or understanding what was happening in the brain”. Freeman was also co-founder and president of the American Board of Psychiatry and Neurology from 1946 to 1947 and a contributor and member of the American Psychiatric Association.
Freeman, W. & Watts, J.W. (1942) Psychosurgery: Intelligence, Emotion and Social Behaviour Following Prefrontal Lobotomy for Mental Disorders. Springfield, Illinois: Charles C. Thomas Publisher.
Robert E. Valett
Robert E. Valett (22 November 1927 to 14 November 2008) was an American psychology professor who wrote more than 20 books primarily focused on educational psychology. He earned the distinguished psychologist award from the San Joaquin Psychological Association and was a president of the California Association of School Psychologists.
Early Life and Education
Robert Edward Valett was born in Clinton, Iowa on 22 November 1927. His father, Edward John Valett, worked for the railroad as a pipe fitter and his mother, Myrtle (née Peterson), was a saleswoman. Valett attended Clinton High School while also achieving the rank of Eagle Scout in the Boy Scouts of America. During World War 2, he served in the US Navy Medical Corps. He then did his undergraduate work at the University of Iowa and George Williams College. Valett went on to earn an MA from the University of Chicago (1951 ) and an (Ed.D.) in educational psychology from the University of California in Los Angeles.
Valett was a professor of psychology at Orange Coast College in Costa Mesa, Ca., and the University of Canterbury in New Zealand and taught psychology from 1970 to 1992 at California State University, Fresno where he was named Professor Emeritus. He authored several books on learning disabilities, child development, dyslexia and attention disorders/hyperactivity. He received the distinguished psychologist award from the San Joaquin Psychological Association in 1982 and served as president of the California Association of School Psychologists from 1971 to 1972.
In 1950, Valett married Shirley Bellman with whom he had 5 children. He died on 14 November 2008, in Fresno, California.
The Remediation of Learning Disabilities – Fearon Publishers 1967.
A Psychoeducational Inventory of Basic Learning Abilities – Fearon Publishers 1968.
Developmental Task Analysis – 1969.
Programming Learning Disabilities – Fearon 1969.
Modifying Children’s Behaviour: A Guide for Parents and Professionals – Fearon 1969.
The Effect of Exercise on Mental Health: A Focus on Inflammatory Mechanisms.
A growing body of research suggests that neuropsychiatric disorders are closely associated with a background state of chronic, low-grade inflammation.
This insight highlights that these disorders are not just localised to dysfunction within the brain, but also have a systemic aspect, which accounts for the frequent comorbid presentation of chronic inflammatory conditions and metabolic syndromes.
It is possible that a treatment resistant subgroup of neuropsychiatric patients may benefit from treatment regimens that target their associated proinflammatory state.
Lifestyle factors such as physical activity (PA) and exercise (i.e. structured PA) are known to influence mental health. In turn, mental disorders may limit health-seeking behaviours – a proposed “bidirectional relationship” that perpetuates psychopathology. PA is renowned for its positive physical, physiological and mental health benefits.
Evidence now points to inflammatory pathways as a potential mechanism for PA in improving mental illness. Relevant pathways include:
Modulation of immune-neuroendocrine and neurotransmitter systems;
The production of tissue-derived immunological factors that alter the inflammatory milieu; and
Neurotrophins that are critical mediators of neuroplasticity.
In this paper, the researchers focus on the role of PA in positively improving mental health through potential modulation of chronic inflammation, which is often found in individuals with mental disorders.
In a related paper by Edirappuli and colleagues (2020), they will focus on the role of nutrition (another significant lifestyle factor) on mental health.
Thus, inflammation appears to be a central process underlying mental illness, which may be mitigated by lifestyle modifications.
Lifestyle factors are advantageous as first-line interventions due to their cost efficacy, low side-effect profile, and both preventative and therapeutic attributes.
By promoting these lifestyle modifications and addressing their limitations and barriers to their adoption, it is hoped that their preventative and remedial benefits may galvanize therapeutic progress for neuropsychiatric disorders.
Venkatesh, A., Edirappuli, S.D., Zaman, H.P. & Zaman, R. (2020) The Effect of Exercise on Mental Health: A Focus on Inflammatory Mechanisms. Psychiatira Danubina. 32(Suppl 1), pp.105-113.
The Effect of Nutrition on Mental Health: A Focus on Inflammatory Mechanisms.
Neuropsychiatric disorders are closely associated with a persistent low-grade inflammatory state.
This suggests that the development of psychopathology is not only limited to the brain, but rather involves an additional systemic aspect, accounting for the large body of evidence demonstrating co-presentation of mental illness with chronic inflammatory conditions and metabolic syndromes.
Studies have shown that inflammatory processes underlie the development of neuropsychiatric symptoms, with recent studies revealing not only correlative, but causative relationships between the immune system and psychopathology.
Lifestyle factors such as diet and exercise may influence psychopathology, and this may occur via a bidirectional relationship.
Mental illness may prevent health-seeking behaviours such as failing to maintain a balanced diet, whilst adopting a ‘healthy’ diet rich in fruits, vegetables and fish alongside nutritional supplementation correlates with a reduction in psychiatric symptoms in patients.
Obesity and the gut microbiome have proven to be further factors which play an important role in inflammatory signalling and the development of psychiatric symptoms.
In a related paper the authors focus on the role of exercise (another significant lifestyle factor) on mental health (Venkatesh et al. 2020).
Lifestyle modifications which target diet and nutrition may prove therapeutically beneficial for many patients, especially in treatment-resistant subgroups.
The current evidence base provides equivocal evidence, however future studies will prove significant, as this is a highly attractive therapeutic avenue, due to its cost efficacy, low side effect profile and preventative potential.
By promoting lifestyle changes and addressing the limitations and barriers to adoption, these therapies may prove revolutionary for mental health conditions.
Edirappuli, S.D., Venkatesh, A. & Zaman, R. (2020) The Effect of Nutrition on Mental Health: A Focus on Inflammatory Mechanisms. Psychiatria Danubina. 32(Suppl 1), pp.114-120.
From Family Surroundings to Intestinal Flora, A Literature Review Concerning Epigenetic Processes in Psychiatric Disorders.
Some behaviours or psychiatric conditions seem to be inherited from parents or explain by family environment.
The researchers hypothesised interactions between epigenetic processes, inflammatory response and gut microbiota with family surroundings or environmental characteristics.
The researchers searched in literature interactions between epigenetic processes and psychiatric disorders with a special interest for environmental factors such as traumatic or stress events, family relationships and also gut microbiota.
They searched on Pubmed, PsycINFO, PsycARTICLES and Sciencedirect articles with the keywords psychiatric disorders, epigenome, microbiome and family relationships.
Some gene polymorphisms interact with negative environment and lead to psychiatric disorders.
Negative environment is correlated with different epigenetic modifications in genes implicated in mental health. Gut microbiota diversity affect host epigenetic.
Animal studies showed evidences for a transgenerational transmission of epigenetic characteristics.
The findings support the hypothesis that epigenetic mediate gene-environment interactions and psychiatric disorders.
Several environmental characteristics such as traumatic life events, family adversity, psychological stress or internal environment such as gut microbiota diversity and diet showed an impact on epigenetic.
These epigenetic modifications are also correlated with neurophysiological, inflammatory or hypothalamic-pituitary-adrenal axis dysregulations.
Dubois, T., Reynaert, C., Jacques, D., Lepiece, B. & Zdanowicz, N. (2020) From Family Surroundings to Intestinal Flora, A Literature Review Concerning Epigenetic Processes in Psychiatric Disorders. Psychiatria Danubina. 32(Suppl 1), pp.158-163.
Protein intake is associated with cognitive functioning in individuals with psychiatric disorders.
Schizophrenia and bipolar disorder are associated with reduced cognitive functioning which contributes to problems in day-to-day functioning and social outcomes.
A paucity of research exists relating dietary factors to cognitive functioning in serious mental illnesses, and results are inconsistent.
The study aims to describe the nutritional intake of persons with schizophrenia and those with a recent episode of acute mania and to determine relationships between the intake of protein and other nutrients on cognitive functioning in the psychiatric sample.
Persons with schizophrenia and those with acute mania were assessed using a 24-h dietary recall tool to determine their intakes of protein and other nutrients.
They were also assessed with a test battery measuring different domains of cognitive functioning. Results indicate that lower amounts of dietary protein intake were associated with reduced cognitive functioning independent of demographic and clinical factors.
The association was particularly evident in measures of immediate memory and language.
There were not associations between cognitive functioning and other nutritional variables, including total energy, gluten, casein, saturated fat, or sugar intakes.
The impact of dietary interventions, including protein intake, on improving cognitive functioning in individuals with psychiatric disorders warrants further investigation.
Dickerson, F., Gennusa, J.V. 3rd, Stallings, C., Origoni, A., Katsafanas, E., Sweeney, K., Campbell, W.W. & Yolken, R. (2019) Protein intake is associated with cognitive functioning in individuals with psychiatric disorders. Psychiatry Research. doi: 10.1016/j.psychres.2019.112700. [Epub ahead of print].
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