Neuropsychology Exam Notes.

Learning Objectives

• L01: Describe the training, responsibilities, and assessment methods of a neuropsychologist.
• L02: Explain the major characteristics of:
  • Alzheimer's disease
  • Frontotemporal neurocognitive disorder
  • Neurocognitive disorder with Lewy bodies
  • Vascular disease
  • Traumatic brain injury
  • Substance/medication-induced neurocognitive disorder
  • Neurocognitive disorder due to HIV infection
  • Neurocognitive disorder due to prion disease
• L03: Describe the features of:
  • Tumors
  • Infections
  • Epilepsy
  • Multiple sclerosis
  • Migraine headaches
• L04: Explain the basic principles that predict recovery from brain damage.
• L05: Describe the major methods used to treat neurocognitive disorders.

What Is Neuropsychology?

• Neuropsychology is a specialty within clinical psychology focused on understanding and treating patients with cognitive impairments resulting from aging, disease, or injury.

Who Are the Neuropsychologists?

• Neuropsychologists are licensed doctoral-level (PhD or PsyD) clinical psychologists who have completed specialized training.
• They are expected to understand the relationships between the nervous system and behavior.
• Many seek board certification from organizations such as the American Academy of Clinical Neuropsychology (AACN) or the American Board of Clinical Neuropsychology (ABCN).
• Organizations are working with the American Psychological Association (APA) to standardize curricula for neuropsychology specialization.
• Neuropsychologists often collaborate with neurologists and neurosurgeons:
  • Neurologists and neurosurgeons assess and treat the physical consequences of disease or injury.
  • Neuropsychologists assess and treat the cognitive consequences.
  • Example: For a soldier with a concussion,
    • Neurologist/neurosurgeon would address bleeding and swelling.
    • Neuropsychologist would assess cognitive functioning and provide rehabilitation for attention span and working memory changes.

Neuropsychological Assessment

• Similar to other psychological assessments, neuropsychological assessments use standardized instruments to evaluate behavior.
• Careful assessment of cognitive and behavioral strengths and weaknesses can lead to an informed treatment plan.
• The choice of test depends on the goals and the patient's condition.
  • Comparing scores to population norms: Useful for distinguishing intellectual disability from dyslexia.
  • Determining impact of illness or injury: Compare performance on affected vs. unaffected abilities; e.g., Broca's area stroke impacting language production more than visual perception.
• Test selection can be specific to the patient. Comprehensive instruments like the Halstead-Reitan battery (intellect, sensation, motor function, attention, psychological disorder) offer good reliability but can be too long for severely injured patients.

Behavioral Neuroscience Working as Clinical Neuropsychologist

• Training involves a PhD or PsyD in clinical psychology with licensure, followed by a foundation in neurosciences (neurology, neuroanatomy, neurophysiology).
• After the doctoral degree, a minimum of 2 years of supervised training in neuropsychology is required.
• Specialization in child (pediatric) or adult neuropsychology is common, with 2-3 years of additional experience expected before board certification.

Neurocognitive Disorders

• Most neurological conditions have cognitive consequences, ranging from mild to major.
• Neurocognitive disorder is diagnosed when a patient experiences a decline in functioning in one or more cognitive domains (attention, executive function, learning and memory, perception and movement, or social cognition) due to a known challenge to the central nervous system.
• These disorders are acquired, not present since birth.
• Major neurocognitive disorder is distinguished from minor based on severity and interference with independent living.
• The term dementia is often applied to major neurocognitive disorders, especially those associated with older age.
• Parkinson's and Huntington's disease were explored in Chapter 8.
• The text will follow the DSM-5-TR outline for studying conditions that can cause neurocognitive disorder.

Alzheimer Disease

• Alzheimer's disease (AD) is a major cause of dementia, affecting approximately 50 million people worldwide.
• Rates increased due to longer life expectancy but have recently declined in some wealthier countries (USA, UK, France), possibly due to lifestyle factors, education, and better treatments for related conditions.
• Prevalence increases dramatically with age, affecting <1% before 65 and 27% in those over 90.
• African-Americans experience nearly double the rates of AD observed in white Americans, possibly due to environmental factors.
• AD begins with mild memory loss, especially episodic memory. Problem-solving, language, and social behavior deteriorate as the disease progresses, and the patient begins to experience severe symptoms of hallucination and delusional thinking. Eventually, basic life skills deteriorate, and the person needs careful supervision and care. Prior to death, many patients are unable to move or speak.
• An obvious challenge to obtaining valid test results is the likelihood that the very condition for which individuals are being tested can affect their test performance. Factors such as pain, fatigue, depression, test anxiety, medications, and motivation can easily distort results on standardized tests such as IQ tests.
• Standard neuropsychological assessments fail to take advantage of recent technologies. Wearables, household sensors, and virtual assistants could provide extensive, ecologically valid data, although privacy concerns must be addressed. New, culturally validated instruments are assisting neuropsychologists in the diagnosis of neurocognitive disorders in racially and ethnically underrepresented communities

Abnormal Structures and Proteins

• Neurofibrillary tangles: A hallmark feature; made of detached tau (τ) protein molecules that normally stabilize microtubules. Without tau, microtubules collapse, and the neuron deteriorates.
• Beta Amyloid: Contributes to tau detachment and collects in amyloid plaques (abnormal patches) on axons and blood vessels. Individuals with Down syndrome, who have three copies of chromosome 21, frequently experience these same characteristic abnormalities because the APP gene is located on chromosome 21.

The Amyloid Hypothesis Controversy

• In 2006, it was claimed that a subtype of beta amyloid transferred symptoms of AD to otherwise healthy young rats.
• Subsequent lack of success in developing medications led to the questioning of the amyloid hypothesis.
• In 2022, evidence of image tampering in the original paper was discovered.
• Whether amyloid plaques are causal or simply an effect of other disease processes remains unknown.

Diagnostic Measures and Genetics

• No cures exist, but early identification can slow down progression, so biomarkers found in CSF and blood are helpful in identifying earlier stages of Alzheimer's disease. PET scans targeting amyloid proteins and MRI scans indicating small blood vessel disease are also used to identify probable Alzheimer's disease.
• Definitive diagnosis requires an autopsy, but probable AD is diagnosed based on genetic testing, family history, learning and memory impairments, and a steady loss of cognitive function.
• In rare cases, AD is inherited as a dominant trait due to mutations in genes for:
  • Amyloid Precursor Protein (APP) on chromosome 21
    APP (chromosome 21)
  • Presenilin 1 (PSEN1) on chromosome 14
    PSEN1 (chromosome 14)
  • Presenilin 2 (PSEN2) on chromosome 1
    PSEN2 (chromosome 1)
• The age of onset in these cases is as many as 40 years earlier than cases due to other causes.
• The ε4 variant of the apolipoprotein E (APOE) gene, located on chromosome 19 is the most reliable genetic risk factor. People with an ε4 allele have higher cholesterol levels and more arteriosclerotic plaques, increasing their risk for cardiovascular disease and stroke in addition to dementia.
  • The ε3 allele is the most common, followed by ε4 and ε2
  • 91% of people who are homozygous for the ε4 allele are likely to be diagnosed with AD at an average age of 68.
  • 47% of heterozygotes with one ε4 allele will be diagnosed at the average age of 76.
  • 20% of people with no ε4 alleles will be diagnosed at an average age of 84.
• The ε2 allele appears to convey some protection from Alzheimer's disease.
• Genotypes interact with other factors:
  • Non-exercisers with other APOE alleles had a greater risk of Alzheimer disease than exercisers.

Ethical Considerations: The Amyloid Hypothesis

• Alzheimer's disease presents a perfect storm for potential scientific misconduct because it affects large numbers of people at staggering costs to families, communities, and nations and because there has been little, if any, progress toward effective treatments.
• Alzheimer disease research has been characterized by an intense debate between proponents of the amyloid hypothesis and those who point the causal finger at tau proteins.
• Adopting strong open science practices is always helpful, but more is needed. Funding agencies, university administrators, and perhaps most importantly, patients and their loved ones, must be patient and realistic in their expectations.

Cellular Changes in Alzheimer’s Disease

• Synapse Loss: Correlates with cognitive functioning in AD patients. Synapses that are performing poorly might be tagged by microglia for elimination, enhancing the rate of loss.
• Disruption of the endosomal-lysosomal network (ELN): ELN, a critical component in the cell’s ability to clear itself of toxins and debris. Disruptions in lysosome activity can lead to the accumulation of cellular waste and problems with neurochemical release and the recycling of synaptic vesicles. The breakdown of lysosome membranes can lead to the death of neurons and microglia.
• Oxidative Stress: Disrupts the brain’s ability to manage oxidative stress. The nature of the phospholipid neural membrane makes neurons particularly vulnerable to attack by free radicals.
• Disruption in the functioning of microRNAs (miRNA): Loss of the ability to protect normal functioning, which rather characterizes Alzheimer disease not so much as the result of pathological influences but rather as the result of the failure of normal protective mechanisms.

Network Effects & Treatments for AD

• The damage to the brains of patients with AD follows a characteristic pattern. Cognitive symptoms are highly correlated to the progression of the disease through networks, producing a cascading network failure because of transneuronal degeneration.
• Neurofibrillary tangles caused by tau pathology are first observed in the entorhinal cortex.
• Beta amyloid accumulates within the default mode network (DMN) and reduced connectivity within the DMN.
• Treatments for AD:
  • No treatments reverse the course of AD; current medications only slow the progression by about six months.
  • Approved medications include acetylcholinesterase inhibitors and an NMDA receptor antagonist.
  • Aducanumab (Aduhelm): Acts as an antibody to beta amyloid. The causal role of beta amyloid in AD is now in doubt, and the medication’s reputation has been damaged further.
  • Many institutionalized patients with AD are treated with antipsychotic medications to reduce aggressiveness, but this practice is associated with earlier death.

Frontotemporal Neurocognitive Disorder

• Frontotemporal neurocognitive disorder, or frontotemporal dementia (FTD), is a group of syndromes featuring degeneration of the frontal and temporal lobes, usually on the left hemisphere.
• FTD is rare but is the most common form of dementia in people under 60. About 15% of patients with amyotrophic lateral sclerosis (ALS) will also be diagnosed with FTD.
• Cases typically fall into one of three groups:
  • Behavioral: Personality changes and loss of social cognition (50% of FTD cases).
  • Semantic: Language difficulties, remains fairly fluent, but loses memory for the meanings of words.
  • Nonfluent: Experiences difficulty with speech production.
• Genetics play a significant role in the development of FTD. Thirty percent of patients have a strong family history of the disorder. A number of genes associated with FTD are also related to neuroinflammation and possible autoimmune processes.
• Current treatments target the reduction of the severity of symptoms but do not improve the condition itself. Drugs under investigation include those that address pathological tau and the effects of genetic mutations associated with FTD.
• One of the odd correlates of FTD is a sudden increase in artistic interest and ability on the part of some patients. It is possible that damage to the left frontal and parietal cortices disinhibits the activity of the right hemisphere in these patients. Temporary increases in artistic ability similar to those found in cases of FTD can be established by applying repeated transcranial magnetic stimulation (rTMS) to the left fronto-parietal junction.

Neurocognitive Disorder with Lewy Bodies

• Lewy bodies are clumps of misfolded alpha-synuclein protein that disrupt neural functioning.
• Lewy bodies are found in neurocognitive disease with Lewy bodies (NCDLB) and Parkinson disease.
• Together, these Lewy body diseases make up the second most frequent cause of dementia following Alzheimer disease.
• The two disorders are usually distinguished by the timing of symptoms. In Parkinson disease, motor symptoms typically precede the appearance of dementia symptoms by one year or more. In NCDLB, cognitive symptoms generally precede any motor deficits.
• Most of the Lewy bodies in NCDLB are located in the limbic system, while those in Parkinson disease aggregate in the brainstem. Individuals with NCDLB experience frequent hallucinations, which typically do not occur until late stages in Alzheimer disease and other dementias.
• Unlike Alzheimer disease, which produces a steady decline without plateaus, NCDLB symptoms often come and go. Patients with NCDLB also frequently experience REM sleep behavior disorder.
• The causes of NCDLB remain unclear, although patients with this condition share overlapping genetic profiles with those who have Alzheimer disease or Parkinson disease. Treatments are provided to manage symptoms. As in other dementias, cholinesterase inhibitors slow the progression of symptoms slightly.
• About half of patients with NCDLB possess a hypersensitivity to antipsychotic medications, producing life-threatening consequences.

Vascular Disease (Stroke)

• The cells of the nervous system are unable to rely on stored supplies of oxygen, which is delivered to the brain by a rich network of blood vessels. The circulation of blood to neural tissue can be interrupted by ruptures and blockages of the blood vessels serving the brain.
• A stroke occurs when the brain’s blood supply is interrupted by either hemorrhage (bleeding) or by the sudden blockage of a blood vessel. Risk factors for stroke include age, hypertension (high blood pressure), smoking, diabetes, high cholesterol levels, obesity, poor diet, lack of exercise, air pollution, and alcohol use.
• Worldwide, stroke is the second most frequent cause of death and the leading cause of permanent disability. Over 12 million new strokes, or one every second, occur each year.
• Cerebral hemorrhage, or bleeding in the brain, generally results from hypertension or structural defects in the arteries serving the brain or from blood diseases such as leukemia or exposure to toxic chemicals.
• Blockages of blood vessels result in ischemia, or low oxygen levels. Ischemia often results in the death of neural tissue, producing an area known as an infarct. Infarcts can cause changes in consciousness, sensation, or the ability to move, depending on their size and location.
• Transient ischemic attacks (TIAs) produce brief episodes (24 hours or less) of stroke symptoms and are strong predictors of subsequent stroke.
• Material causing the blockage of a blood vessel can be classified as either a thrombosis or an embolism.

Ischemia and Excitotoxicity

• Autopsy results of patients who died following ischemia indicated that only certain cells appeared to be damaged.
• It was discovered that excess glutamate can kill neurons.
• Cell death following strokes is largely caused by excess glutamate activity triggered by disruptions in the delivery of oxygen.
• In response to unusual amounts of glutamate, abnormal calcium activity in the cell stimulates four “executioner” enzymes that damage the cell’s energy stores, membranes, cytostructure, and DNA.
• Treatment for ischemic strokes can include thrombolysis, or the dissolution of blood clots using medication, or endovascular treatment, in which a clot is removed through a microcatheter inserted in the arm or groin.
• Prompt medical attention can save many other neurons and glia in the ischemic penumbra, the area immediately surrounding an infarct.

Traumatic Brain Injury (TBI)

• Traumatic brain injuries (TBIs) are the result of physical damage to the brain. Leading causes of TBI include traffic accidents, gunshot wounds, assault, and falls. Increasing numbers of military personnel and civilians in war zones have experienced TBI as a result of blast injuries.
• The severity of TBI can be categorized into mild, moderate, or severe, usually based on a version of the Glasgow Coma Scale (GCS), duration of loss of consciousness, and brain imaging.

Types of TBI

• Traumatic brain injuries can be divided into two categories: Open head injuries involve penetration of the skull, while concussions, or closed head injuries, do not.
• Blast injuries can produce both open and closed head injuries and produce symptoms similar to those of other types of TBI, with a few major exceptions.
• Severe swelling, disruption of the blood–brain barrier, and major damage to the blood supply are more frequently observed in military as opposed to civilian cases of TBI. Imaging studies identify frequent white matter disruptions, cerebellum damage, and thalamic network damage. A history of blast TBI is often associated with PTSD, anxiety, depression, sleep disorders, attention disorders, and cognitive disorders.
• A concussion occurs in response to a blow to the head or to another part of the body, resulting in “impulsive” force being transmitted to the brain. Concussions can range from mild (no or very brief periods of unconsciousness) to severe (resulting in coma).

Recognizing the Signs of a Stroke Using BEFAST

• Because treatment for stroke is more effective within three hours of onset, it is important to know the outward signs of a stroke. You can remember the symptoms using the BEFAST acronym:
  • B is for balance
  • E is for eyes (problems with vision)
  • F is for face drooping
  • A is for arm weakness
  • S is for speech difficulty
  • T is for time to call 9-1-1 to summon help

Coup and Countercoup

• At the site of a blow, known as the coup, the brain might be damaged by compression of the skull against the neural tissue. The force of the blow pushes the brain against the side of the skull opposite the coup, producing a second area of damage known as the countercoup. A severe coup or countercoup might be accompanied by bleeding, or subdural (under the dura mater) hematoma.
• Pressure exerted on the brain by the swelling of injured tissues produces additional damage and interruptions in normal functioning.
• Repeated TBI is a significant risk factor for neurocognitive disease. A “punch drunk” syndrome, later referred to as dementia pugilistica (boxer’s syndrome), was first identified in professional boxers. Today, these repetitive injuries are usually known as chronic traumatic encephalopathy (CTE).

Outcomes and Treatment of TBI

• Behavioral and cognitive consequences of TBI vary widely. Cortical functions normally taking place at the location of the damage or in related networks are affected adversely.
• When symptoms extend beyond the “acute” or immediate timeframe of the injury, the patient is diagnosed with major or mild neurocognitive disorder due to traumatic brain injury and occur more frequently in patients with previous TBI and/or preinjury psychological disorders.
• Many medications are used to address the wide-ranging behavioral and neurocognitive symptoms of TBI. Stimulants are often used to address memory and attention issues. Antidepressants and antianxiety medications are used in cases with mood-related symptoms. Additional rehabilitation methods, including the use of virtual reality (VR), are discussed later in this chapter.

Substance/Medication-Induced Neurocognitive Disorder

• A number of recreational and therapeutic drugs produce symptoms of neurocognitive disorder outside the actual intoxication or withdrawal periods associated with a drug. The drugs that are particularly likely to result in neurocognitive disorder are alcohol, cocaine, methamphetamine, opioids, phencyclidine (PCP), sedatives, hypnotics, antianxiety drugs, and solvents.
• Several types of drugs produce specific effects that are capable of independently producing neurocognitive deficits.
  • Methamphetamine increases the risk for vascular accidents and damages the blood–brain barrier.
  • Alcohol abuse is associated with nutritional deficits and can lead to amnestic confabulatory (Korsakoff) neurocognitive disorder, in which patients experience problems learning new information and recalling both recent and distant events, although other cognitive processing appears relatively normal.

Neurocognitive Disorder Due to HIV Infection

• Acquired immune deficiency syndrome (AIDS) is a set of symptoms and infections resulting from the damage to the human immune system caused by the human immunodeficiency virus (HIV).
• NCD due to HIV infection, results either directly from the actions of the HIV virus itself or from other opportunistic infections that overwhelm the impaired immune system of the patient with HIV.
• The action of the HIV virus on neural cell death is indirect because HIV directly invades macrophages, microglia, astrocytes, and the vascular endothelial cells that line the blood vessels serving the brain, not neurons themselves.
• Antiretroviral treatments carry their own risk of producing neurocognitive disorders.

Neurocognitive Disorder Due to Prion Disease

• Among the most dramatic neurocognitive disorders are the transmissible spongiform encephalopathies (TSEs), a group that includes bovine spongiform encephalopathy (BSE), or mad-cow disease. Human TSEs include Creutzfeld-Jakob disease (CJD), kuru, and fatal familial insomnia.
• The symptoms common to this group of diseases are devastating: psychological disturbances, including paranoia, anxiety, and depression in humans and skittishness in herd animals; progressive loss of cognitive function; motor disturbances; and finally death.
• Stanley Prusiner (1982) proposed that TSEs were caused by a new type of infectious agent, a single protein, which he named a prion.
• Another piece of the TSE puzzle fell into place during the 1950s, when scholars investigated a disease known as kuru, which affected the Fore people of New Guinea, and was eventually traced to the Fore’s practice of cannibalism.

Prion Proteins Have Normal and Abnormal Forms

• The abnormal version, PrPsc, is the cause of TSEs and can change the structure of normal PrPc, spreading the condition throughout the nervous system.

Connecting to Research - Stanley Prusiner and the Prion

• One of the challenges Prusiner faced was the long incubation time of a TSE, which ran contrary to the demands of granting agencies and academic promotion policies. Switching from mice to Syrian hamsters and refining his methods helped him speed up the process. Brain tissue from infected animals was tested with multiple methods used to identify proteins and viruses.
• The scrapie agent was inactivated by methods that break down proteins but remained unaffected by five methods known to modify nucleic acids. Based on these observations, Prusiner rejected the possibility that the infectious agent was a virus, plasmid, or viroid, and instead identified the agent as a protein he called a prion.
• In recognition of Prusiner’s efforts, which he maintained despite often strident criticism, he was awarded the Nobel Prize in Physiology or Medicine in 1997.

BSE and Variant Creutzfeldt-Jakob Disease (vCJD)

• The BSE epidemic resulted from changes in procedures for producing animal feed and has caused more than 143 in the UK to die from vCJD.

Neurocognitive Disorders Due to Other Medical Conditions

• The DSM-5-TR includes a number of disorders in the “due to other medical conditions” category:
  • Brain tumors
  • Hydrocephalus
  • Oxygen deficits following cardiac arrest
  • Endocrine conditions
  • Nutritional conditions
  • Infectious diseases
  • Immune disorders
  • Kidney failure
  • Metabolic conditions
  • Epilepsy
  • Multiple sclerosis
• Migraine headaches have an indirect relationship with neurocognitive disorder because they increase a person’s risk for stroke and interact with existing psychological disorders.

Brain Tumors

• Tumors, which are independent growths of new tissue that lack purpose, originate in the brain itself (primary tumors), while secondary tumors result from metastasis.
• There are general symptoms due to increased pressure within the skull and specific disruptions related to the location of the tumor.
• They are identified according to the tissue from which they arise:
  • Gliomas: Develop in glial cells and account for more than 70% of brain tumors.
  • Meningiomas: Arise within the tissues of the meninges and are typically easy to remove surgically because they lie on the surface of the brain instead of invading the tissue within the brain.
• The WHO classifies tumors from Grade I (least serious) to Grade IV (most serious).
• The most common approach to brain tumors is surgical removal. In addition to surgery, or in cases in which surgery is very risky or impossible, whole brain radiation is used. Hyperthermia, a noninvasive approach using lasers or magnetism, allows physicians to use heat to damage the tissue of the tumor.
• Alternate chemotherapy agents are being developed that either interfere with the blood–brain barrier or bypass it completely. Researchers have also implanted dissolving, chemotherapy-releasing wafers during surgery to remove tumors.

Infections

• Certain infections circumvent the formidable protection surrounding the brain and nervous system. The neurocognitive consequences of such invasions are dramatic, and many of these disorders are life threatening.

Parasites

• The most common parasitic infection affecting the central nervous system is neurocysticercosis and results from infection with the eggs of the pork tapeworm, Taenia solium, usually through the ingestion of fecal material from a symptom-free tapeworm carrier in the household. Fluid-filled cysts, approximately one to two cm in diameter, form around the larvae.
• Treatment generally consists of medication for seizure control. If the cysts still harbor a live worm, treatment with antiworm (anthelminthic) medications can be useful.

Bacterial, Viral, and Fungal Infections

• Encephalitis is an inflammation of the brain caused by viral infection and results from two modes of infection: Primary encephalitis and Secondary encephalitis.
• Meningitis is an inflammation of the meninges that results from infection by bacteria, viruses, or fungi. It produces flulike symptoms (elevated temperature, vomiting, diarrhea, etc.) and can be distinguished from the flu by the presence of neck stiffness, aversion to bright lights, and drowsiness.

Epilepsy

• Seizures are uncontrolled electrical disturbances in the brain that are correlated with changes in consciousness, and can be diagnosed using EEGs.
• Types of Seizures:
  • Partial seizures vs. Generalized seizures.
  • Simple partial seizures: Cause movements or sensations appropriate to the location of the starting point/focus, not accompanied by changes in consciousness.
  • Complex partial seizures: Begin in the temporal lobes, associated with alterations in consciousness.
• Patterns within a Seizure
  • The paroxysmal depolarizing shift (PDS):
    • begins with a large, abrupt depolarization of affected neurons that triggers a train of action potentials
    • is followed by a period of hyperpolarization.
      GABA mediated inhibitory system is overwhelmed leading to high frequency discharges of action potentials.
  • Tonic-clonic seizures: loss of consciousness, cessation of breathing, and intense muscular contraction.
  • Absence seizures: Much less violent, person loses consciousness for about 10 seconds with motor movements limited to blinking, head turns, and eye movements.

Treatment for Epilepsy

• Medications used to treat epilepsy are known as antiepileptic drugs, or AEDs. Many AEDs act as GABA agonists, although others target sodium and calcium channels. If medications are not effective, surgery might be indicated.

Multiple Sclerosis

• Multiple sclerosis (MS) is an autoimmune condition in which the immune system attacks the central nervous system. Specifically, MS damages oligodendrocytes, leading to the sclerosis, or scarring, that gives the disorder its name, and to the demyelination of axons.
• A key environmental factor related to MS is exposure to the Epstein-Barr virus, responsible for mononucleosis.
• Although no cure has been found for MS, a number of medications reduce the severity of attacks and slow the progression of the disease.

Migraine

• Migraine produces symptoms of excruciating head pain, nausea, and vomiting for a period of four to 72 hours.
• The leading hypothesis for the cause of migraine headaches is the trigeminovascular theory, which suggests that headaches are the result of inflammation from the release of factors by the trigeminal vascular system.
• CGRP are released by the trigeminal nerve (cranial nerve V), producing dilation of the blood vessels and pain.
• Observations that people treated with Botox for cosmetic purposes also experienced headache relief led to investigations into the use of Botox to treat migraine.

Recovery and Treatment in Neurocognitive Disorders

• Although much central nervous system damage is permanent, recovery of behavioral function can still occur in cases of neurocognitive disorder.

Plasticity and Recovery

• Plasticity refers to the brain’s ability to reorganize, forming the basis of development and learning and promoting recovery from brain damage in two general ways:
  • Reactive or functional neuroplasticity where functions like language are moved from a damaged to an undamaged part of the brain and requires spontaneous changes in cortical excitability, metabolic rate, or blood flow to support new functions.
  • Structural neuroplasticity where changes occur due to learning. By providing appropriate learning opportunities, rehabilitation can enhance the brain’s ability to learn new ways to carry out functions affected by brain damage.
• In addition to observations of youthful plasticity in humans, the Kennard Principle is supported by animal research. Goldman-Rakic and Rakic (1984) removed an entire occipital lobe from a rhesus monkey in utero, leading to a dramatic structural reorganization (refer to Figure 15.27).

Cognitive Reserve

• Cognitive reserve is the brain’s resilience in the face of age-related changes and damage from variables, including: IQ, educational and occupational status, and engagement in enriching leisure activities.
• Rehabilitation literally means “to restore to good health.”

Rehabilitation for Neurocognitive Disorders

• Three factors that must be addressed include changes in cognitive abilities, emotional changes, and physical changes.
• Methods to improve cognitive function use one of two methods:
  • Cognitive approach (top-down):
    • Advocates stressing a particular cognitive function, such as attention.
  • A functional approach:
    • Focuses on specific tasks rather than cognitive skills.
• Virtual Reality can be utilized
  • Allows patients to participate in therapy for as long as they want without aid from expensive staff.
  • Enhances recovery indirectly through improved motivation and enjoyment.
  • Incorporating using Wii-hab gaming system in rehabilitation.