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COMPLETE Introduction to Neuroscience Notes [Version 2 - Part 4] - got 90% on final

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Department
Neuroscience
Course
CAS NE 101
Professor
All Professors
Semester
Fall

Description
Clinical Neurology 11/15/2013 Deductive reasoning is important Diagnosis obtained in 80% of patients by history alone Physical examination and localization confirm 10% of diagnoses Diagnostic testing: another 5% The rest we don’t know What is the problem (history) Localization allows for more rapid diagnosis and treatment MRIs are very inaccurate (bright spot abnormalities) Cerebrum­  Higher cortical functions Right hemisphere damage Constructional apraxia (cant draw things) damage to the right hemisphere Hemineglect of the left field Anisognosia­ don’t know anything’s wrong with you Left hemisphere Cant write Motor aphasia Receptive aphasia Visual system Formed visual misperceptions Pallinopsia­ you see things that you were just looking at in other places Photopsia Metamorphopsia­ human faces look stretched and distorted Basal ganglia Abnormal muscle tone (dystonia, ridigity) Involuntary movements (tremor, hypokinetic, akinesia, akathesia, chorea, athetosis, ballismus) Decreased arm swing Abnormal gait Limbic system Level of alertness Emotional responses Memory Sexual behavior Feeding and metabolic homeostasis Endocrine function Brainstem Midbrain Weakness, eye beating movements= midbrain lesion Pons Multiple sclerosis, damage of the myelin of the brain paths Sensoroy loss, dizziness, ataxia, difficulty swallowing and chewing Medulla Difficulty swallowing Coma is uncommon Motor and sensory impairment Cerebellum Midline/vermis hemispheres  Controls endpoint of the finger (shaky point) Right Upper motor neuron weakness (weakness) Inhibits increased tone muscle (face>arm>leg) Left Right sided weakness Pronator drift Holding arm out in front of your body, one arm will be stable and one wont Spinal cord Anterior cord: motor Twitching, decreased reflexes,  Posterior Localization on certain parts of spinal cord Dermatomes Pin pricking on body, to find where the lesion is  Plexus Flail arm­ caught during birth In upper chest Peripheral nerves polyneuropathy Decreased reflexes Distal weakness Diabetic neuropathy­ fingers toes get numb Toxic neuropathy­ lead, arsenic Mononeuropathy Focal weakness Carpal tunnel, syndrome, peroneal palsy Neuromuscular junction Symmetric weakness Normal reflexes Fluctuating severity Sensation intact Muscle disorder (myopathy) Proximal Normal bowel control Elevated muscle enzymes in blood Neuroimaging MRI usually superior to CT Imaging is not a substitute for the examination EEg Epilepsy Children Brain death Blood work Neuroimaging in Alzheimer’s Disease 11/15/2013 Neuroimaging in Alzheimer’s Disease 11/15/2013 Cortical atrophy Temporal lobes, frontal lobe Extreme shrinkage in the hippocampus Ventricles get a lot larger Grey matter atrophy Amyloid beta Plaques are formed in AD Lead to cell death (outside the cell) Tau protein involved in transporting nutrients to distant parts of neurons the tau tangles up (inside the cell) Genes involved Amyloid precursor protein Early onset Neuroimaging in Alzheimer’s Disease 11/15/2013 Presenilin 1 (early onset) Presenilin 2 (early and late onset) ApoE4 (late onset) Treatment Cholinesterase inhibitors ▯ inhibits enzyme that breakdown acetocholine Memantine Limits neurons’ sentitivity to glutamate, which can reduce cell death caused by glutamate excitoxicity no drug that have been shown to be effective treatment Disease progression Early stages Mild cognitive impairment 20 yrs. Before diagnosis plaques and tangles begin to form learning/memory/thinking/planning impaired Mild to Moderate Memory problems begin to interfere with daily life General confusion Trouble expression thoughts Neuroimaging in Alzheimer’s Disease 11/15/2013 Speech/understanding impairment Proprioceptive trouble Personality changes Severe Most of the cortex is seriously damaged Brain shrinks dramatically due to cell death Lose ability to communicate/care for themselves/recognize family members High amyloids are not a good indicator of future ALZ Structural MRI Software that allows you to trace grey/white matter surface Measure of cortical thickness  ▯ correlates to number of neurons CHRONIC TRAUMATIC ENCHEPHALOPATHY (CTE) Caused by TBI Diffuse axonal injury Mechanical tissue damage ▯ cells get squished ▯ cell death Neuroimaging in Alzheimer’s Disease 11/15/2013 Reduced blood flow Neuronal dysfunction Diffuse trauma Tangles near the surface of cortex Symptoms  Irritability Depression and suicidal thoughts Increased aggression Memory loss Decreased executive function, unable to plan for future Some motor dysfunctions Speech slurring and dysfunction confusion Clinical talks 11/15/2013 complex partial seizure­ one side of the brain MONEY IS THE ONLY IMPORTANT FACTOR IS LIFE DECISIONS FUCK FEMINISM, HE SAYS Pain management Someone just died on his hands Pathophysology ▯ Migrane Probably selective in evolution to help you Aura is caused by a speading wave of depolarization, “cortical spreading depression” Slow moving Before migrane sets in Vessels dialate ▯ throbbing headache Treatment Avoidance of triggers Early RX of acute attacks Most migraines are not due to only one trigger Big doses, taken early (abortive) Using more than one, or two abortive drug is advised­ stepwise, to avoid one med class overuse Dementia 11/15/2013 Dementia 11/15/2013 The number of people dying of dementia has increased Because there are more older people alive Diabetes increases the chance of dementia Delaying onset 5 years could severely help the progression of the disease What is Dementia A syndrome Something acquired loss of cognitive and emotional abilities Interferes with work or usual social activities Insidious onset, persistent, progressive DSM­V proposes new name Major Neurocognitive Disorder Mild Cognitive Impairment Mild acquired decline in cognitive abilities Noted subjectivity and/or with objectively documented decline Not affecting fu
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