Bneuro ch 15: Neuropsychology

neuropsychology

a specialty field within clinical psychology that seeks to understand and treat patients with cognitive impairments resulting from: aging, disease, or injury

neuropsychologist

licensed doctoral level clinical psychologists who complete specialized training. they often work in collaboration with neurologists

standardized tests

• comparisons with population

• comparisons with abilities unaffected by condition

• IQ tests

• Halstead-Reitan battery

neuropsychological assessment

goal to develop an informed treatment plan, choice of methods depends on the issues involved but usually uses standardized tests, and condition might affect test performance.

neurocognitive disorders

described in the DSM 5. they are diagnosed when a patient experiences a decline in functioning in one or more cognitive domains after a known challenge to the nervous system(attention, executive function, learning and memory, perception and movement, and social cognition).

tumors

independent growths of new tissue that lack purpose. most are infiltrating, they grow diffusely through surrounding tissue. about 10% are metastatic.

metastatic

about 10% of brain tumors, they originate elsewhere, usually the lungs

primary tumors of the brain

rare, causes unknown, but radiation is a risk

secondary tumors of the brain

arise from glial cells, meninges, and ependymal cells. it is the most common type of tumor until age 19

malignant tumor

a cancerous tumor that can cause harm. it lacks a distinct border and may metastasize. it is likely to return after removal.

benign tumor

a noncancerous tumor that does no harm. it has a distinct border that cannot metastasize

symptoms of brain tumors

• pressure in the skul

• headache, vomiting, double vision, reduced heart rate, reduced alertness, and seizures

• specific disruptions related to location

treatment for tumors

• surgical removal

• whole brain radiation

• stereotaxic radiosurgery

• ultrasound therapy

• chemotherapy limited by BBB

• thalidomide to starve tumors of blood supply

• experimental delivery of stem cells with anticancer genes

gliomas

a cancerous brain tumor type composed of one of several types of glial cells. more than 70% of brain tumors.

meningiomas

abnormal cell growth within the meninges. 20% of brain tumors. they are encapsulated, usually benign, and more prone to successful surgical removal.

stroke

a sudden-onset cerebrovascular event that causes brain damage. 5th leading cause of death in the US and most common cause of adult disability

infarction

obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue

cerebral hemorrhage

bleeding in the brain-blood vessel ruptures

cerebral ischemia

disruption of blood supply.

• thrombosis

• embolism

• arteriosclerosis

arteriosclerosis

wall of blood vessels thicken, usually due to fat deposits

embolism

plug forms elsewhere and moves to the brain

thrombosis

plug forms

transient ischemic attack (TIA)

mini strokes, no permanent damage

aneurysm

a weakened point in a blood vessel that makes a stroke. may be congenital or due to poison or infection.

congenital

present at birth

damage due to cerebral ischemia

does not develop immediately. most damage is a consequence of excess neurotransmitter release (glutamate). blood-deprived neurons become overactive and release glu. glu over activates its receptors, especially NMDA receptors leading to an influx of Na+ and Ca++

influx of Na and Ca triggers

release of still more glutamate, and a sequence of internal reactions that ultimately kill the neuron - apoptosis

ischemia-induced brain damage

takes time (about 10 mins), does not occur equally in all parts of the brain, and mechanisms of damage vary with the brain structure affected.

NMDA antagonists

block damage of cerebral ischemia

chronic traumatic encephalopathy (CTE)

a dementia type syndrome resulting from multiple consussions

closed-head injuries

brain injuries due to blows that do not penetrate teh skull - the brain collides with the skull

contrecoup injuries

contusions are often on the side of the brain opposite to the blow. bundles of axons can be torn and twisted, blood vessels can be ruptured, and cerebrospinal fluid can distort the walls of the ventricles. traumatic brain injury can be followed several months later by a chronic seizure disorder

contusions

closed-head injuries that involve damage to the cerebral circulatory system

hematoma

clotted blood in an organ or tissue. a bruise will form

concussion

when there is a disturbance of conscious head and no evidence of structural damage

brain infection

invasion of the brain by microorganisms

encephalitis

the resulting inflammation of brain infection

bacterial infections

often leads to cerebral abscesses, pockets of pus. may imflame meninges, creating meningitis. can be treated with penicillin and other antibiotics

viral infections

attack neural tissues

syphilis

a bacterial causes of brain infections. may produce a syndrome of insanity and dementia. bacteria are passed to the noninfected and enter a dormant stage for years

rabies

a viral infection. high affinity for the nervous system

mumps and herpes

a viral infection. typically attack tissues other than the brain

zika virus

a viral infection. it can be transferred from pregnant women to fetus, leading to microcephaly (small head size)

neurotoxins

may enter general circulation from the GI tract, lungs, or through the skin.

toxic psychosis

chronic insanity produced by a neurotoxin. 18-19th century hat makers had toxic psychosis due to mercury exposure

tardive dyskinesis

a motor disorder produced by some antipsychotic drugs.

neurotoxic effects of alcohol

thiamine deficiency, may cause brain damage

endogenous

produced by the body (includes some neurotoxins that attack the body)

epilepsy

The primary symptom is seizures, but not all who have seizures have epilepsy. epileptics have seizures generated by their own brain dysfunction. affects 1% of the population. difficult to diagnose due to the diversity and complexity of the epileptic seizures.

convulsions

motor seizures

• tremors

• rigidity

• loss of balance and consciousness

causes of epilepsy

brain damage or genes (over 70 so far)

how to diagnosis epilepsy

EEG - electroencephalogram

seizures associated with high amplitude spikes 

seizures

often preceded by an aura, such as a smell, hallucination, or feeling.

partial epilepsy

does not involve the whole brain

generalized epilepsy

involve the entire brain

treatment of seizures

often treated with anticonvulsants (benzodiazepines - GABA action)

simple partial seizures

symptoms are primarily sensory or motor or both. symptoms spread as epileptic discharge spreads

complex simple seizures

often restricted to the temporal lobes (temporal lobe epilepsy). The patient engages in compulsive and repetitive simple behaviors - automatisms. more complex behaviors seem norma. 

grand mal seizures

• loss of consciousness and equilibrium

• tonic-clonic convulsions

• resulting hypoxia may cause brain damage

petit mal (absence) seizures

• not associated with convulsions

• a disruption of consciousness associated with a cessation of ongoing behavior

typical treatment for generalized seizures

antiepileptic medications (benzos)

benzos

GABA antagonists

multiple sclerosis

a progressive disease (autoimmune disorder) that attacks CNS myelin, leaving areas of hard scar tissue (sclerosis). nature and severity of deficits vary with the nature, size, and position of sclerotic lesions. periods of remission are common. symptoms include visual disturbances, muscle weakness, numbness, tremor, and loss of motor coordination (ataxia). drugs may retard progression or block some symptoms.

multiple sclerosis epidemiology

• women are 3x likely than men to have it

• rare amongst africans and asians

• increased in those who spend childhood in a cool climate

treatments for multiple sclerosis

1. interferon B

2. glatiramer acetate

They are only effective for the remitting-relapse form of MS, not the progressive form

glatiramer acetate

a mixture of synthetic peptides composed from random sequences of the amino acids tyrosine, glutamate, alanine, and lysine to treat MS. This compound was first produced in an attempt to induce the symptoms of MS in lab animals, but it turned out to actually reduce them.

interferon B

a protein that modulates the responsiveness of the immune system. It reduces the frequency and severity of attacks and slows the progression of neurological disabilities in some patients with MS

Alzheimer’s disease

the most common cause of dementia, the likelihood of developing it increases with age.

10% over 65, and 50% over 85

it is progressive, with early stage characterized by confusion and a selective decline in memory. definitive diagnosis only at autopsy—must observe neurofibrillary tangles and amygloid plaques

alzheimer’s biological causes

all infected genes are involved in synthesis of amyloid or tau (look like black tiny dots on the brain), a protein found in the tangles. declined acetylcholine levels is among one of earliest changes seen

which comes first, amyloid plaques or neuro-fibrillary tangles?

amyloid

tau protein

serves as a component of microtubules, which provide the cell’s transport mechanism. during the progression of alzheimer’s excessive amounts of phosphate ions become attached to strands of tau protein, thus changing its molecular structure. abnormal filaments are seen in the soma and porximal dendrites of cells in the cerebral cortex, which disrupts transport of substances within the cell. the cell dies, leaving behind a tangle of protein filaments

transgenic

genes of another species have been introduced

genes accelerating human amyloid synthesis introduced into mice

• plague distrubution comparable to that in AD

• no neurofibrillary tangles

• mice showed deficits in memory tasks indicating it results in an AD behavioral phenotype

parkinson’s disease

a movement disorder of middle and old age affecting 1-2% of the elderly population. it is 2.5x more likely in males than females. pain and depression commonly seen before the full disorder develops. tremor at rest is the common common symptom, and they also have frozen facial expressions. dementia is not typically seen, and there is not single cause.

potential causes of parkinson’s

• genetics role in early-onset

• exposure to environmental toxins

• head injury

• correlation with lack of coffee use

damage from parkinson’s disease

dopaminergic neurons of the substantia nigra begin to degenerate (low dopamine). linked to about 10 different gene mutations. they tend to disrupt the function of mitochondria but are seen in the rare familial early onset form.

L-dopa

dopamine precurser that can temporarily treat parkinson’s

lewy bodies

abnormal circular structures found within the cytoplasm. (protein clumps) in the DA neurons of the substania nigra in parkinson’s

Parkinson’s treatments

• deep brain stimulation (only treats motor sympotms)

• brain lesions of globus pallidus (averse side effects)

• GAD (glutamic acid decarboxylase) - the enzyme responsible for the biosynthesis of GABA

• implant fetal stem cells into the basal ganglia (severe dyskinesia)

Huntington’s disease

a progressive motor disorder of middle and old age, but rare, with a strong genetic basis. associated with dementia. begins with figetiness and progresses to jerky movements of entire limbs and severe dementia. Death usually occurs within 15 years of symptoms, first symptoms usually not seen until age 40.

cause of Huntington’s disease

caused by a single gene on chromosome 4 and degeneration of the caudate and putamen (BG)

huntingtin (HTT)

protein that may serve to facilitate the production and transport of brain-derived neurotrophic factor. abnormal HTT becomes misfolded and forms aggregations that accumulate in the caudate, triggering apoptosis in the cell.

early huntington’s disease

associated with longer glutamine, indicates that this abnormal portion of the HTT molecules is responsible for the disease

huntington’s repeated sequence of bases

gene defect, the code ofr the amino acid glutamine. it causes the gene product (HTT) to contain an elongated stretch of glutamine. the longer the sequence (more repeats), the earlier symptoms will show up.

migrainees

symptoms of excruciating head pain, nausea, and vomiting for 4-72 hours. the risk is much higher for women then men. migraine generator located in brainstem

treatment for migraines

• triptans prevent release of CGRP

• botox injections (back of neck, forehead, and side of head above ear)

• behavioral adjustments