Neuroanatomy – Mental Health Matters

What is Neuroprotection?

Published on 09/27/202309/27/2023 by Andrew Marshall1 Comment

Introduction

Neuroprotection refers to the relative preservation of neuronal structure and/or function.

In the case of an ongoing insult (a neurodegenerative insult) the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation. It is a widely explored treatment option for many central nervous system (CNS) disorders including neurodegenerative diseases, stroke, traumatic brain injury, spinal cord injury, and acute management of neurotoxin consumption (i.e. methamphetamine overdoses). Neuroprotection aims to prevent or slow disease progression and secondary injuries by halting or at least slowing the loss of neurons.

Despite differences in symptoms or injuries associated with CNS disorders, many of the mechanisms behind neurodegeneration are the same. Common mechanisms of neuronal injury include decreased delivery of oxygen and glucose to the brain, energy failure, increased levels in oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory changes, iron accumulation, and protein aggregation. Of these mechanisms, neuroprotective treatments often target oxidative stress and excitotoxicity—both of which are highly associated with CNS disorders. Not only can oxidative stress and excitotoxicity trigger neuron cell death but when combined they have synergistic effects that cause even more degradation than on their own. Thus limiting excitotoxicity and oxidative stress is a very important aspect of neuroprotection.

Common neuroprotective treatments are glutamate antagonists and antioxidants, which aim to limit excitotoxicity and oxidative stress respectively.

Excitotoxicity

Glutamate excitotoxicity is one of the most important mechanisms known to trigger cell death in CNS disorders. Over-excitation of glutamate receptors, specifically NMDA receptors, allows for an increase in calcium ion (Ca²⁺) influx due to the lack of specificity in the ion channel opened upon glutamate binding. As Ca²⁺ accumulates in the neuron, the buffering levels of mitochondrial Ca²⁺ sequestration are exceeded, which has major consequences for the neuron. Because Ca²⁺ is a secondary messenger and regulates a large number of downstream processes, accumulation of Ca²⁺ causes improper regulation of these processes, eventually leading to cell death. Ca²⁺ is also thought to trigger neuroinflammation, a key component in all CNS disorders.

Glutamate Antagonists

Glutamate antagonists are the primary treatment used to prevent or help control excitotoxicity in CNS disorders. The goal of these antagonists is to inhibit the binding of glutamate to NMDA receptors such that accumulation of Ca²⁺ and therefore excitotoxicity can be avoided. Use of glutamate antagonists presents a huge obstacle in that the treatment must overcome selectivity such that binding is only inhibited when excitotoxicity is present. A number of glutamate antagonists have been explored as options in CNS disorders, but many are found to lack efficacy or have intolerable side effects. Glutamate antagonists are a hot topic of research. Below are some of the treatments that have promising results for the future:

Estrogen: 17β-Estradiol helps regulate excitotoxicity by inhibiting NMDA receptors as well as other glutamate receptors.
Ginsenoside Rd: Results from the study show ginsenoside rd attenuates glutamate excitotoxicity. Importantly, clinical trials for the drug in patients with ischemic stroke show it to be effective as well as noninvasive.
Progesterone: Administration of progesterone is well known to aid in the prevention of secondary injuries in patients with traumatic brain injury and stroke.
Simvastatin: Administration in models of Parkinson’s disease have been shown to have pronounced neuroprotective effects including anti-inflammatory effects due to NMDA receptor modulation.
Memantine: As a low-affinity NMDA antagonist that is uncompetitive, memantine inhibits NMDA induced excitotoxicity while still preserving a degree of NMDA signalling.
Riluzole is an antiglutamatergic drug used to slow the progression of amyotrophic lateral sclerosis.

Oxidative Stress

Increased levels of oxidative stress can be caused in part by neuroinflammation, which is a highly recognised part of cerebral ischemia as well as many neurodegenerative diseases including Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis. The increased levels of oxidative stress are widely targeted in neuroprotective treatments because of their role in causing neuron apoptosis. Oxidative stress can directly cause neuron cell death or it can trigger a cascade of events that leads to protein misfolding, proteasomal malfunction, mitochondrial dysfunction, or glial cell activation. If one of these events is triggered, further neurodegradation is caused as each of these events causes neuron cell apoptosis. By decreasing oxidative stress through neuroprotective treatments, further neurodegradation can be inhibited.

Antioxidants

Antioxidants are the primary treatment used to control oxidative stress levels. Antioxidants work to eliminate reactive oxygen species, which are the prime cause of neurodegradation. The effectiveness of antioxidants in preventing further neurodegradation is not only disease dependent but can also depend on gender, ethnicity, and age. Listed below are common antioxidants shown to be effective in reducing oxidative stress in at least one neurodegenerative disease:

Acetylcysteine: It targets a diverse array of factors germane to the pathophysiology of multiple neuropsychiatric disorders including glutamatergic transmission, the antioxidant glutathione, neurotrophins, apoptosis, mitochondrial function, and inflammatory pathways.
Crocin: Derived from saffron, crocin has been shown to be a potent neuronal antioxidant.
Oestrogen: 17α-oestradiol and 17β-oestradiol have been shown to be effective as antioxidants. The potential for these drugs is enormous. 17α-oestradiol is the non-oestrogenic stereoisomer of 17β-oestradiol. The effectiveness of 17α-oestradiol is important because it shows that the mechanism is dependent on the presence of the specific hydroxyl group, but independent of the activation of oestrogen receptors. This means more antioxidants can be developed with bulky side chains so that they do not bind to the receptor but still possess the antioxidant properties.
Fish oil: This contains n-3 polyunsaturated fatty acids that are known to offset oxidative stress and mitochondrial dysfunction. It has high potential for being neuroprotective and many studies are being done looking at the effects in neurodegenerative diseases.
Minocycline: Minocycline is a semi-synthetic tetracycline compound that is capable of crossing the blood brain barrier. It is known to be a strong antioxidant and has broad anti-inflammatory properties. Minocyline has been shown to have neuroprotective activity in the CNS for Huntington’s disease, Parkinson’s disease, Alzheimer’s disease, and ALS.
PQQ: Pyrroloquinoline quinone (PQQ) as an antioxidant has multiple modes of neuroprotection.
Resveratrol: Resveratrol prevents oxidative stress by attenuating hydrogen peroxide-induced cytotoxicity and intracellular accumulation of ROS. It has been shown to exert protective effects in multiple neurological disorders including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and ALS as well as in cerebral ischemia.
Vinpocetine: Vinpocetine exerts neuroprotective effects in ischaemia of the brain through actions on cation channels, glutamate receptors and other pathways. The drop in dopamine produced by vinpocetine may contribute to its protective action from oxidative damage, particularly in dopamine-rich structures. Vinpocetine as a unique anti-inflammatory agent may be beneficial for the treatment of neuroinflammatory diseases. It increases cerebral blood flow and oxygenation.
THC: Delta 9-tetrahydrocannabinol exerts neuroprotective and antioxidative effects by inhibiting NMDA neurotoxicity in neuronal cultures exposed to toxic levels of the neurotransmitter, glutamate.
Vitamin E: Vitamin E has had varying responses as an antioxidant depending on the neurodegenerative disease that it is being treated. It is most effective in Alzheimer’s disease and has been shown to have questionable neuroprotection effects when treating ALS. A meta-analysis involving 135,967 participants showed there is a significant relationship between vitamin E dosage and all-cause mortality, with dosages equal to or greater than 400 IU per day showing an increase in all-cause mortality. However, there is a decrease in all-cause mortality at lower doses, optimum being 150 IU per day. Vitamin E is ineffective for neuroprotection in Parkinson’s disease.

Stimulants

NMDA receptor stimulants can lead to glutamate and calcium excitotoxicity and neuroinflammation. Some other stimulants, in appropriate doses, can however be neuroprotective.

Selegiline: It has been shown to slow early progression of Parkinson’s disease and delayed the emergence of disability by an average of nine months.
Nicotine: It has been shown to delay the onset of Parkinson’s disease in studies involving monkeys and humans.
Caffeine: It is protective against Parkinson’s disease. Caffeine induces neuronal glutathione synthesis by promoting cysteine uptake, leading to neuroprotection.

Neuroprotectants (Cerebroprotectants) for Acute Ischemic Stroke

When applied to protecting the brain from the effects of acute ischemic stroke, neuroprotectants are often called cerebroprotectants. Over 150 drugs have been tested in clinical trials, leading to the regulatory approval of tissue plasminogen activator in several countries, the and approval of edaravone in Japan.

Other Neuroprotective Treatments

More neuroprotective treatment options exist that target different mechanisms of neurodegradation. Continued research is being done in an effort to find any method effective in preventing the onset or progression of neurodegenerative diseases or secondary injuries. These include:

Caspase inhibitors: These are primarily used and studied for their anti apoptotic effects.
Trophic factors: The use of trophic factors for neuroprotection in CNS disorders is being explored, specifically in ALS. Potentially neuroprotective trophic factors include CNTF, IGF-1, VEGF, and BDNF.
Therapeutic hypothermia: This is being explored as a neuroprotection treatment option for patients with traumatic brain injury and is suspected to help reduce intracranial pressure.
Erythropoietin has been reported to protect nerve cells from hypoxia-induced glutamate toxicity (see erythropoietin in neuroprotection).
Lithium exerts neuroprotective effects and stimulates neurogenesis via multiple signaling pathways; it inhibits glycogen synthase kinase-3 (GSK-3), upregulates neurotrophins and growth factors (e.g., brain-derived neurotrophic factor (BDNF)), modulates inflammatory molecules, upregulates neuroprotective factors (e.g., B-cell lymphoma-2 (Bcl-2), heat shock protein 70 (HSP-70)), and concomitantly downregulates pro-apoptotic factors. Lithium has been shown to reduce neuronal death, microglial activation, cyclooxygenase-2 induction, amyloid-β (Aβ), and hyperphosphorylated tau levels, to preserve blood-brain barrier integrity, to mitigate neurological deficits and psychiatric disturbance, and to improve learning and memory outcome.
Neuroprotection D1 and other neuroprotections and certain resolvins of the D series (i.e. RvD1, RvD2, RvD3, RvD4, RvD5, and RvD6) are docosanoid metabolites of the omega 3 fatty acid, docosahexaenoic acid (DHA) while resolvins of the E series (RvD1, RvD2, and RvD3) are eicosanoid metabolites of the omega 3 fatty acid, eicosapentaenoic acid (EPA). These metabolites, which are made by the action of cellular lipoxygenase, cyclooxygenase, and/or cytochrome P450 enzymes on DHA or EPA, have been shown to have potent anti-inflammation activity and to be neuroprotective in various models of inflammation-involving neurological diseases such as various degenerative diseases including Alzheimer’s disease. A metabolically resistant analogue of RvE1 is in development for the treatment of retinal disease and neuroprotection D1 mimetics are in development for treatment of neurodegenerative diseases and hearing loss.

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What is Clinical Neuropsychology?

Published on 06/21/2021 by Andrew MarshallLeave a comment

Introduction

Clinical neuropsychology is a sub-field of psychology concerned with the applied science of brain-behaviour relationships.

Clinical neuropsychologists use this knowledge in the assessment, diagnosis, treatment, and or rehabilitation of patients across the lifespan with neurological, medical, neurodevelopmental and psychiatric conditions, as well as other cognitive and learning disorders. The branch of neuropsychology associated with children and young people is paediatric neuropsychology.

Clinical neuropsychology is a specialised form of clinical psychology. Strict rules are in place to maintain evidence as a focal point of treatment and research within clinical neuropsychology. The assessment and rehabilitation of neuropsychopathologies is the focus for a clinical neuropsychologist. A clinical neuropsychologist must be able to determine whether a symptom(s) may be caused by an injury to the head through interviewing a patient in order to determine what actions should be taken to best help the patient. Another duty of a clinical neuropsychologist is to find cerebral abnormalities and possible correlations. Evidence based practice in both research and treatment is paramount to appropriate clinical neuropsychological practice.

Assessment is primarily by way of neuropsychological tests, but also includes patient history, qualitative observation and may draw on findings from neuroimaging and other diagnostic medical procedures. Clinical neuropsychology requires an in-depth knowledge of: neuroanatomy, neurobiology, psychopharmacology and neuropathology.

Brief History

During the late 1800s, brain-behaviour relationships were interpreted by European physicians who observed and identified behavioural syndromes that were related with focal brain dysfunction.

Clinical neuropsychology is a fairly new practice in comparison to other specialty fields in psychology with history going back to the 1960s. The specialty focus of clinical neuropsychology evolved slowly into a more defined whole as interest grew. Threads from neurology, clinical psychology, psychiatry, cognitive psychology, and psychometrics all have been woven together to create the intricate tapestry of clinical neuropsychology, a practice which is very much so still evolving. The history of clinical neuropsychology is long and complicated due to its ties to so many older practices. Researchers like Thomas Willis (1621-1675) who has been credited with creating neurology, John Hughlings Jackson (1835-1911) who theorised that cognitive processes occurred in specific parts of the brain, Paul Broca (1824-1880) and Karl Wernicke (1848-1905) who studied the human brain in relation to psychopathology, Jean Martin Charcot (1825-1893) who apprenticed Sigmund Freud (1856-1939) who created the psychoanalytic theory all contributed to clinical medicine which later contributed to clinical neuropsychology. The field of psychometrics contributed to clinical neuropsychology through individuals such as Francis Galton (1822-1911) who collected quantitative data on physical and sensory characteristics, Karl Pearson (1857-1936) who established the statistics which psychology now relies on, Wilhelm Wundt (1832-1920) who created the first psychology lab, his student Charles Spearman (1863-1945) who furthered statistics through discoveries like factor analysis, Alfred Binet (1857-1911) and his apprentice Theodore Simon (1872-1961) who together made the Binet-Simon scale of intellectual development, and Jean Piaget (1896-1980) who studied child development. Studies in intelligence testing made by Lewis Terman (1877-1956) who updated the Binet-Simon scale to the Stanford-Binet intelligence scale, Henry Goddard (1866-1957) who developed different classification scales, and Robert Yerkes (1876-1956) who was in charge of the Army Alpha and Beta tests also all contributed to where clinical neuropsychology is today.

Clinical neuropsychology focuses on the brain and goes back to the beginning of the 20th century. As a clinician a clinical neuropsychologist offers their services by addressing three steps: assessment, diagnosis, and treatment. The term clinical neuropsychologist was first made by Sir William Osler on 16 April 1913. While clinical neuropsychology was not a focus until the 20th century evidence of brain and behaviour treatment and studies are seen as far back as the neolithic area when trephination, a crude surgery in which a piece of the skull is removed, has been observed in skulls. As a profession, clinical neuropsychology is a subspecialty beneath clinical psychology. During World War I (1914-1918) the early term shell shock was first observed in soldiers who survived the war. This was the beginning of efforts to understand traumatic events and how they affected people. During the Great Depression (1929-1941) further stressors caused shell shock like symptoms to emerge. In World War II (1939-1945) the term shell shock was changed to battle fatigue and clinical neuropsychology became even more involved with attempting to solve the puzzle of peoples’ continued signs of trauma and distress. The Veterans Administration or VA was created in 1930 which increased the call for clinical neuropsychologists and by extension the need for training. The Korean War (1950-1953) and Vietnam War (1960-1973) further solidified the need for treatment by trained clinical neuropsychologists. In 1985 the term post-traumatic stress disorder or PTSD was coined and the understanding that traumatic events of all kinds could cause PTSD started to evolve.

The relationship between human behaviour and the brain is the focus of clinical neuropsychology as defined by Meir in 1974. There are two subdivisions of clinical neuropsychology which draw much focus; organic and environmental natures. Ralph M. Reitan, Arthur L. Benton, and A.R. Luria are all past neuropsychologists whom believed and studied the organic nature of clinical neuropsychology. Alexander Luria is the Russian neuropsychologist responsible for the origination of clinical psychoneurological assessment after WWII. Building upon his original contribution connecting the voluntary and involuntary functions influencing behaviour, Luria further conjoins the methodical structures and associations of neurological processes in the brain. Luria developed the ‘combined motor method’ to measure thought processes based on the reaction times when three simultaneous tasks are appointed that require a verbal response. On the other side, environmental nature of clinical neuropsychology did not appear until more recently and is characterised by treatments such as behaviour therapy. The relationship between physical brain abnormalities and the presentation of psychopathology is not completely understood, but this is one of the questions which clinical neuropsychologists hope to answer in time. In 1861 the debate over human potentiality versus localisation began. The two sides argued over how human behaviour presented in the brain. Paul Broca postulated that cognitive problems could be caused by physical damage to specific parts of the brain based on a case study of his in which he found a lesion on the brain of a deceased patient who had presented the symptom of being unable to speak, that portion of the brain is now known as Broca’s Area. In 1874 Carl Wernicke also made a similar observation in a case study involving a patient with a brain lesion whom was unable to comprehend speech, the part of the brain with the lesion is now deemed Wernicke’s Area. Both Broca and Wernicke believed and studied the theory of localisation. On the other hand, equal potentiality theorists believed that brain function was not based on a single piece of the brain but rather on the brain as a whole. Marie J.P Flourens conducted animal studies in which he found that the amount of brain tissue damaged directly affected the amount that behaviour ability was altered or damaged. Kurt Goldstein observed the same idea as Flourens except in veterans who had fought in World War I. In the end, despite all of the disagreement, neither theory completely explains the human brains complexity. Thomas Hughlings Jackson created a theory which was thought to be a possible solution. Jackson believed that both potentiality and localisation were in part correct and that behaviour was made by multiple parts of the brain working collectively to cause behaviours, and Luria (1966-1973) furthered Jackson’s theory.

The Role

When considering where a clinical neuropsychologist works, hospitals are a common place for practitioners to end up. There are three main variations in which a clinical neuropsychologist may work at a hospital; as an employee, consultant, or independent practitioner. As a clinical neuropsychologist working as an employee of a hospital the individual may receive a salary, benefits, and sign a contract for employment. In the case of an employee of a hospital the hospital is in charge of legal and financial responsibilities. The second option of working as a consultant implies that the clinical neuropsychologist is part of a private practice or is a member of a physicians group. In this scenario, the clinical neuropsychologist may work in the hospital like the employee of the hospital but all financial and legal responsibilities go through the group which the clinical neuropsychologist is a part of. The third option is an independent practitioner whom works alone and may even have their office outside of the hospital or rent a room in the hospital. In the third case, the clinical neuropsychologist is completely on their own and in charge of their own financial and legal responsibilities.

Assessment

Assessments are used in clinical neuropsychology to find brain psychopathologies of the cognitive, behavioural, and emotional variety. Physical evidence is not always readily visible so clinical neuropsychologists must rely on assessments to tell them the extent of the damage. The cognitive strengths and weaknesses of the patient are assessed to help narrow down the possible causes of the brain pathology. A clinical neuropsychologist is expected to help educate the patient on what is happening to them so that the patient can understand how to work with their own cognitive deficits and strengths. An assessment should accomplish many goals such as; gage consequences of impairments to quality of life, compile symptoms and the change in symptoms over time, and assess cognitive strengths and weaknesses. Accumulation of the knowledge earned from the assessment is then dedicated to developing a treatment plan based on the patient’s individual needs. An assessment can also help the clinical neuropsychologist gauge the impact of medications and neurosurgery on a patient. Behavioural neurology and neuropsychology tools can be standardised or psychometric tests and observational data collected on the patient to help build an understanding of the patient and what is happening with them. There are essential prerequisites which must be present in a patient in order for the assessment to be effective; concentration, comprehension, and motivation and effort.

Lezak lists six primary reasons neuropsychological assessments are carried out: diagnosis, patient care and its planning, treatment planning, treatment evaluation, research and forensic neuropsychology. To conduct a comprehensive assessment will typically take several hours and may need to be conducted over more than a single visit. Even the use of a screening battery covering several cognitive domains may take 1.5-2 hours. At the commencement of the assessment it is important to establish a good rapport with the patient and ensure they understand the nature and aims of the assessment.

Neuropsychological assessment can be carried out from two basic perspectives, depending on the purpose of assessment. These methods are normative or individual. Normative assessment, involves the comparison of the patient’s performance against a representative population. This method may be appropriate in investigation of an adult onset brain insult such as traumatic brain injury or stroke. Individual assessment may involve serial assessment, to establish whether declines beyond those which are expected to occur with normal aging, as with dementia or another neurodegenerative condition.

Assessment can be further subdivided into sub-sections:

History Taking

Neuropsychological assessments usually commence with a clinical interview as a means of collecting a history, which is relevant to the interpretation of any later neuropsychological tests. In addition, this interview provides qualitative information about the patient’s ability to act in a socially apt manner, organise and communicate information effectively and provide an indication as to the patient’s mood, insight and motivation. It is only within the context of a patient’s history that an accurate interpretation of their test data and thus a diagnosis can be made. The clinical interview should take place in a quiet area free from distractions. Important elements of a history include demographic information, description of presenting problem, medical history (including any childhood or developmental problems, psychiatric and psychological history), educational and occupational history (and if any legal history and military history).

Selection of Neuropsychological Tests

It is not uncommon for patients to be anxious about being tested; explaining that tests are designed so that they will challenge everyone and that no one is expected to answer all questions correctly may be helpful. An important consideration of any neuropsychological assessment is a basic coverage of all major cognitive functions. The most efficient way to achieve this is the administration of a battery of tests covering: attention, visual perception and reasoning, learning and memory, verbal function, construction, concept formation, executive function, motor abilities and emotional status. Beyond this basic battery, choices of neuropsychological tests to be administered are mainly made on the basis of which cognitive functions need to be evaluated in order to fulfil the assessment objectives.

Report Writing

Following a neuropsychological assessment it is important to complete a comprehensive report based on the assessment conducted. The report is for other clinicians, as well as the patient and their family so it is important to avoid jargon or the use of language which has different clinical and lay meanings (e.g. intellectually disabled as the correct clinical term for an IQ below 70, but offensive in lay language). The report should cover background to the referral, relevant history, reasons for assessment, neuropsychologists observations of patient’s behaviour, test administered and results for cognitive domains tested, any additional findings (e.g. questionnaires for mood) and finish the report with a summary and recommendations. In the summary it is important to comment on what the profile of results indicates regarding the referral question. The recommendations section contains practical information to assist the patient and family, or improve the management of the patient’s condition.

Educational Requirements of Different Countries

The educational requirements for becoming a clinical neuropsychologist differ between countries. In some countries it may be necessary to complete a clinical psychology degree, before specialising with further studies in clinical neuropsychology. While some countries offer clinical neuropsychology courses to students who have completed 4 years of psychology studies. All clinical neuropsychologists require a postgraduate qualification, whether it be a Masters or Doctorate (Ph.D, Psy.D. or D.Psych).

Australia

To become a clinical neuropsychologist in Australia requires the completion of a 3-year Australian Psychology Accreditation Council (APAC) approved undergraduate degree in psychology, a 1-year psychology honours, followed by a 2-year Masters or 3-year Doctorate of Psychology (D.Psych) in clinical neuropsychology. These courses involve coursework (lectures, tutorials, practicals etc.), supervised practice placements and the completion of a research thesis. Masters and D.Psych courses involve the same amount of coursework units, but differ in the amount of supervised placements undertaken and length of research thesis. Masters courses require a minimum of 1,000 hours (125 days) and D.Psych courses require a minimum of 1,500 hours (200 days), it is mandatory that these placements expose students to acute neurology/neurosurgery, rehabilitation, psychiatric, geriatric and paediatric populations.

Canada

To become a clinical neuropsychologist in Canada requires the completion of a 4-year honours degree in psychology and a 4-year doctoral degree in clinical neuropsychology. Often a 2-year master’s degree is required before commencing the doctoral degree. The doctoral degree involves coursework and practical experience (practicum and internship). Practicum is between 600 and 1,000 hours of practical application of skills acquired in the programme. At least 300 hours must be supervised, face-to-face client contact. The practicum is intended to prepare students for the internship/residency. Internships/residencies are a year long experience in which the student functions as a neuropsychologist, under supervision. Currently, there are 3 CPA-accredited Clinical Neuropsychology internships/residencies in Canada, although other unaccredited ones exist. Prior to commencing the internship students must have completed all doctoral coursework, received approval for their thesis proposal (if not completed the thesis) and the 600 hours of practicum.

United Kingdom

To become a clinical neuropsychologist in the UK, requires prior qualification as a clinical or educational psychologist as recognised by the Health Professions Council, followed by further postgraduate study in clinical neuropsychology. In its entirety, education to become a clinical neuropsychologist in the UK consists of the completion of a 3-year British Psychological Society accredited undergraduate degree in psychology, 3-year Doctorate in clinical (usually D.Clin.Psy.) or educational psychology (D.Ed.Psy.), followed by a 1-year Masters (MSc) or 9-month Postgraduate Diploma (PgDip) in Clinical Neuropsychology. The British Psychological Division of Counselling Psychology are also currently offering training to its members in order to ensure that they can apply to be registered Neuropsychologists also.

United States

In order to become a clinical neuropsychologist in the US and be compliant with Houston Conference Guidelines, the completion of a 4-year undergraduate degree in psychology and a 4 to 5-year doctoral degree (Psy.D. or Ph.D.) must be completed. After the completion of the doctoral coursework, training and dissertation, students must complete a 1-year internship, followed by an additional 2 years of supervised residency. The doctoral degree, internship and residency must all be undertaken at American Psychological Association approved institutions. After the completion of all training, students must apply to become licensed in their state to practice psychology. The American Board of Clinical Neuropsychology, The American Board of Professional Neuropsychology, and The American Board of Paediatric Neuropsychology all award board certification to neuropsychologists that demonstrate competency in specific areas of neuropsychology, by reviewing the neuropsychologist’s training, experience, submitted case samples, and successfully completing both written and oral examinations. Although these requirements are standard according to Houston Conference Guidelines, even these guidelines have stated that the completion of all of these requirements is still aspirational, and other ways of achieving clinical neuropsychologist status are possible.