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Chapter 15

PSYC 211 Chapter 15

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McGill University
PSYC 211
Yogita Chudasama

Chapter 15: Neurological Disorders Focus of chapter: discuss major categories of neuropathological conditions of the brain, including: tumors, seizure disorders, cerebrovascular accidents, disorders of development, degenerative disorders, and disorders caused by infectious diseases. Tumors • A tumor is a mass of cells whose growth is uncontrolled and serves no useful function • Tumors can be: • Malignant (cancerous) – infiltrate surrounding tissue and undergo metastases • Benign (usually harmless) – encapsulated (can be easily removed) • Tumors damage brain tissue by: • Compression by benign tumors • Compression and infiltration by malignant tumors • Tumors DO NOT arise from nerve cells, which are incapable of dividing • They arise from other cells in the brain or from metastases originating elsewhere in the body - The most serious types of tumors are metastases and the gliomas Seizure Disorders • A seizure is a period of sudden, excessive activity of cerebral neurons • If neurons that make up the motor system are involved, a seizure can cause convulsion – wild, uncontrollable activity of muscles • Partial seizures have a definite focus or source of irritation • Neurons involved are restricted to a small part of the brain • Generalized seizures are widespread, involving most of he brain • Simple and complex seizures are 2 categories of partial seizures • Simple partial seizures often cause changes in consciousness but do not cause loss of consciousness • Complex partial seizures cause loss of consciousness • The most severe form of a seizure is referred to as grand mal • It is a generalized seizure involving motor systems of the brain, and thus is accompanied by convulsions • A few seconds before this seizure, the patient experiences an aura caused by the excitation of neurons surrounding the seizure focus • The grand mal seizure begins with the tonic phase where muscles contract forcefully and patient loses consciousness • In the following clonic phase, muscles begin convulsing • After 30 seconds, the patient’s muscles relax and breathing can resume • The patient then falls into an unresponsive sleep for at least 15 minutes • Neural activity during the grand mal seizure: • Neural firing begins at the aura stage • The activity spreads to regions surround the focus then to the contralateral cortex, the basal ganglia, the thalamus, and various nuclei of the brain stem reticular formation • Symptoms begin • Excited cortical regions feed back more excitation to the cortex, amplifying activity • Neurons in the motor cortex begin firing continuously (tonic phase) • Diencephalic structures begin quenching the seizure by sending inhibitory messages to the cortex in bursts then becomes more prolonged until the patient’s muscles relax • Children are susceptible to seizure disorders • They usually have brief spells called absence seizures (petit mal) • An absence is a generalized seizure where the child stares off into the distance for a few seconds blinking rapidly and is unresponsive • Seizures can lead to significant hippocampal damage • Seizures can be caused by scarring, drugs (e.g. alcohol, barbituates), and infections • Seizure disorders are treated with anticonvulsant drugs, which increase inhibitory synapses • After seizure surgery, which involves removal of brain tissue, people’s performance on neuropsychological functioning usually improves • During a seizure, increased excitatory activity is held in check by a compensatory increase in inhibitory activity surrounding the seizure focus known as interictal inhibition • This inhibitory compensation suppresses normal functions of a large region of the brain surrounding the seizure Cerebrovascular Accidents (Strokes) • 2 major types of strokes are hemorrhagic and obstructive: • Hemorrhagic strokes are caused by bleeding within the brain from a malformed blood vessel or one that is weakened by high blood pressure –> blood accumulates in the brain causing damage • Obstructive strokes involve the plugging up of a blood vessel preventing blood flow. The plug can come from a thrombus (blood clot) or an embolus (can come from bacterial debris in the event of an infection) • The immediate cause of neuron death following a stroke is the presence of excessive amounts of glutamate • When blood supply to a region of the brain is interrupted, oxygen and glucose are depleted, and the Na+/K+ transporters stop functioning • Neural membranes become depolarized resulting in the release of glutamate • Glutamate furthers increases the inflow of Na+ ions and causes cells to absorb excessive amounts of Ca2+ through NMDA channels, leading to toxicity • Methods to minimize damage caused by strokes: • Use a drug to dissolve blood clots, such as tPA (however, it has toxic effects to the CNS) • Desmoteplase (an enzyme secreted in the saliva of vampire bats) can restore blood flow and reduce clinical symptoms in a majority of patients if given 9 hours following the stroke • Removal of anterosclerotic plaques by a carotid endarterectomy or the placement of a stent Disorders of Development TOXIC CHEMICALS • Toxins from drugs and viruses can adversely affect fetal development • Mental retardation of the fetus can result from ingestion of alcohol during pregnancy • Fetal alcohol syndrome is characterized by abnormal facial development and deficient brain development • Alcohol disrupts normal brain development by interfering with a neural adhesion protein – one that guides the growth of neurons in the developing brain • Prenatal exposure of alcohol have direct effects on neural plasticity INHERITED METABOLIC DISORDERS • Results from errors in enzyme synthesis • The most common inherited metabolic disorder that can affect brain development is phenylketonuria (PKU) – a disease caused by the lack of an enzyme that converts the amino acid phenylalanine (Phe) into tyrosine • Excessive Phe in the blood interfere with the myelinization of neurons in the CNS, which takes place after birth • PKU can be treated by putting the infant on a low-Phe diet • Pyridoxine dependency results in damage to cerebral white matter, thalamus, and cerebellum • It is treated by large doses of vitamin B6 • Galactosemia is the inability to metabolize galactose (a sugar found in milk) • If not treated, it causes damage to cerebral white matter and cerebellum • Treatment involves a milk substitute that does not contain galactose • Tay-Sachs disease causes the brain to swell and damage itself against the inside of the skull and against the folds of the dura mater • It is a metabolic storage disorder where enzymes involved in waste degradation in lysosomes are missing • Lysosomes increase in size and eventually lead to brain swelling and damage • This disease cannot be easily treated DOWN SYNDROME • A congenital disorder that results in abnormal brain development, producing mental retardation • Caused by an extra chromosome 21 • Incidences increase with increasing maternal age • After the age of 30, the Down syndrome individual’s brain develops abnormal microscopic structures and degenerate, similar to what occurs Alzheimer’s disease • The brain of a Down syndrome patient is approximately 10% lighter than that of a normal person • The convulsions are simpler and smaller • The frontal lobes are small • The superior temporal gyrus is thin • Down syndrome patients can be trained to function well with minimal supervision Degenerative Disorders TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES • Bovine spongiform encephalopathy (mad cow disease) is a transmissible spongiform encephalopathy (TSE) that is contagious that degenerates the brain, giving it a sponge-like appearance • Unlike other transmissible diseases, TSEs are caused not by microorganisms, but by simple proteins called prions • Prions are found in the membrane of neurons where they are believed to play a role in synaptic function • They are resistant to proteolytic enzymes • The infectious prion protein is misfolded and causes normally folded prion proteins to also misfold • The accumulation of misfolded proteins in neurons lead to apoptosis (programmed cell death) facilitated by killer enzymes called caspases PARKINSON’S DISEASE • Caused by degeneration of the nigrostriatal system – the dopamine-secreting neurons of the substantia nigra that send axons to the basal ganglia • Primary symptoms: muscle rigidity, slowness of movement, resting tremor, postural instability • The brains of these patients show near-disappearance of nigrostriatal dopaminergic neurons • Surviving dopaminergic neurons show Lewy bodies (abnormal circular structures found with the cytoplasm) • Mutation of a gene coding for the alpha-synuclein protein on chromosome 4 will produce Parkinson’s disease • This protein is normally found in presynaptic terminals and is involved in synaptic transmission in dopaminergic neurons • The mutation produces a toxic gain of function protein whose effects are toxic to the cell • The mutation is usually dominant • Another hereditary form of Parkinson’s disease is caused by mutation of a gene on chromosome 6 that produces the protein parkin • The mutation causes a loss of function, making this a recessive mutation
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