neuro post midterm Flashcards
Atenolol
B1 adrenergic antagonist. Tx HTN
Salbutamol
B2 adrenergic agonist. Tx asthma (bronchodilator)
Atropine
Muscarinic antagonist. Mydriatic, reduction of drooling in Parkinson’s dz, antidote in poisoning with insecticide
Amyotropic lateral sclerosis (ALS)
Degeneration of anterior horn cells and V, VII, X, XII, parts of pyramidal tract, and primary motor area. Affects LMNs. Flaccid and spastic paralysis. Affects UEs. Decreased cough reflex -> aspiration pneumonia, respiratory insufficiency
Anterior spinal artery (ASA) syndrome
Flaccid paralysis, spastic paresis. Positive Babinski (UMN), lose pain and temp
Central medullary syndrome
I.e. syringomyelia d/t tumors. Lose pain and temp, get flaccid paralysis (no spastic paralysis). Common in cervical spine
Posterior parietal cortex
Brodmann 5+7, integrate sensory info for motor planning in concert w/premotor areas
Lateral corticospinal tract
Mainly flexor. Alpha and gamma. Cortical input. Mainly excitatory
Rubrospinal tract
Flexor. Alpha and gamma. Cortical input. Excitatory
Medullary/lateral reticulospinal tract
Flexor, bilateral innervation. Alpha and gamma via interneuron. Cortical input. Excitatory
Pontine/medial reticulospinal tract
Extensor. Gamma ONLY, via interneuron. Cortical input. Excitatory. Mostly involuntary
Lateral vestibulospinal tract
Extensor. Alpha ONLY, via interneuron. NO CORTICAL INPUT. Vestibular organ - excitatory. Cerebellum - inhibitory
Medial vestibulospinal tract
Extensor. Alpha ONLY. NO CORTICAL INPUT. Inhibition of alpha (glycine). Vestibular organ - excitatory. Cerebellum - inhibitory
Type I motor unit
Slow-twitch; low-tension; fatigue-resistant, aerobic; small motor neuron and axon
Type IIA motor unit
Fast; relatively fatigue-resistant; large tension; some aerobic; relatively large motor neurons
Type II B motor unit
Fast; fatigue-susceptible; large tension; anaerobic; large motor neurons
Dx and tx for myasthenia gravis
Dx - Tensilon test. Tx - azathioprine and corticosteroids - immunosuppressants
Myotonia congenita
Defect in gene encoding Cl- channels, can’t bring Em close to Ecl to recover from AP when K+ is accumulating in TTS -> spontaneous firing of muscles after nerve end stimulation. Prolonged relaxation phase
Ballismus
Due to lesions of subthalamic nucleus. Decreased excitation of GPi -> disinhibition of thalamus and cerebral cortex -> increased contralateral movement
Tardive dyskinesia
D/t antipsychotic drugs (dopamine receptor antagonists), can become permanent
Dopa-induced dyskinesia
Occurs in txt of Parkinson’s w/DOPA -> chorea
Drug-induced Parkinson’s disease
Antipsychotics, depletors of DA stores (ex reserpine), toxic contaminants (MPTP)
Striatal neuronal degeneration and Huntington’s disease
Destruction of striatal neurons expressing D2 receptors -> decreased thalamic inhibition -> increased cortical activity. HYPERKINESIS, CHOREA
Sydenham disease
Chorea d/t autoimmune ABs against striatum resulting from childhood rheumatic fever
Mech of L-DOPA and carbidopa
L-dopa -> increased dopamine synthesis in surviving SNc. Carbidopa -> decreased peripheral metabolism of L-DOPA. Txt w/L-DOPA and carbidopa becomes less effective over several years
Bromocriptine
Stimulates D2 receptors
Pergolide
Stimulates both D1 and D2 receptors
Amantadine
Antiviral drug, may benefit some manifestations of Parkinson’s (akinesia, rigidity) -> ma promote release of dopamine and/or block ACh receptors (also weakly blocks NMDA receptors). Psychiatric SE’s!
Selegiline (deprenyl)
Irreversibly binds MAO B -> may improve responses to or delay need for other therapies
Entacapone and tolcapone
Inhibit COMT -> prolong synaptic longevity of dopamine
Benztropine
Muscarinic antagonist. Block ACh (which has opposite effect of DA on D2) excitation of striatum -> tx resting tremor.
Huntington’s disease
Tx with D2 receptor antagonists -> antichoreic if there’s still surviving D2 striatal neurons or use VMAT inhibitors -> more free dopamine, less stored in vesicles
Louis-Bar syndrome
Widespread degeneration of cerebellar Purkinje cells and compromised immune fxn -> delayed development of motor skills, increased vulnerability to infxn, increased sensitivity to ionizing radiation, bloodshot eyes
Cerebellar cognitive affective syndrome (CCAS)
Cognitive and emotional systems dysfunction resulting from cerebellar injury
Guillain-Barre syndrome
After respiratory or GI infection. Demyelination of peripheral axons. Good recovery, demyelination. Lumbar puncture -> increased protein in CSF. Tx - immunoglobulin
Leprosy (Hansen’s disease)
Prefers unmyelinated axons (pain and temperature). Bacterial multiplication -> compression and ischemia of all peripheral axons. Tx w/multiple abx
Lead poisoning
Focal weakness of extensor muscles of fingers, wrists, and arms. Bilateral arm weakness and wasting in chronic situations. No sensory symptoms. Motor neuropathy in adults and encephalopathy in infants
Alcoholic peripheral neuropathy
First sensory loss, then motor loss (both symmetric). Vit B1 deficiency
Vitamin B1 deficiency
Affects rostral vermis and adjacent parts of anterior lobe. Affects cortical Purkinje cells -> reactive gliosis
DM
Sensory loss (symmetric), motor loss (asymmetric), and autonomic neuropathy. Vasculopathy
Cheyne-Stokes respiration
Lesion in forebrain
Hyperventilation
Lesion in midbrain
Apneusis (inspiratory cramps)
Lesion in pons
Ataxic breathing
Lesion in lower pons/upper medulla
Respiratory arrest
Lesion in medulla (bilateral)
Diencephalic lesion
Small, reactive pupils
Uncal herniation
One dilated, one constricted
Midbrain lesion
Midposition, fixed pupils
Diffuse effects of drugs, metabolic encephalopathy
Small, reactive
Pretectal lesion
Larged, fixed, unreactive
Pontine lesion
Pinpoint pupils
Alexia
Inability to read the left visual field due to dmg in splenium of corpus callosum
Phenytoin, carbamazepine
Tx epilepsy. Block excitation: reduce flow of Na+ and Ca2+ ions into neurons, increase level of GABA, and suppress the release of glutamate -> less excitability
GABAergic, benzodiazepines, barbiturates
Tx epilepsy. Enhance inhibition: potentiate inhibitory GABAa recs and inhibit excitatory AMPA recs
Levetiracetam
Decreases voltage-operated delayed rectifier K+ current w/o effect on Na+ and A-type K+ potassium currents -> reduced repetitive AP generation
Reduction of N-type and P/Q type Ca2+ currents -> decreased NT release
Binds to synaptic vesicle protein, SV2A, which is believed to impede conduction across synapses
Thalamocortical transmission part of ARAS
Cholinergic structures, monoaminergic systems
Lateral hypothalamus, basal forebrain, and cerebral cortex part of ARAS
NA, serotonin, histamine, orexin/hypocretin, ACh, GABA
VLPO in hypothalamus - inhibitory (GABA, galanin), promotes sleep by inhibiting activity in the brain’s arousal centers
Adenosine
Extracellular conc of adenosine rises during waking hours -> inhibits ARAS. During sleep, conc slowly declines. Administration ->NREM sleep
Melatonin
Extracellular conc reaches a max at about2-3am, and declines to low value by 7am. Synthesis: tryptophan->serotonin->melatonin
IL-1
Produced during infections. Conc increases in CSF during NREM. Intraventricular injection -> NREM sleep
Muramyl peptides
From bacterial cell walls. Inject into lateral ventricles of mammals -> NREM sleep
Delta sleep-inducing peptide
Intraventricular injection -> NREM sleep
REM-on cells
Maximally active in REM sleep. Use NTs GABA, glycine, ACh, or glutamate
REM-off cells
Minimally active in REM sleep. Use NTs NE, epi, serotonin, and histamine
Storage areas for procedural, non-declarative memory
Supplementary and premotor cortex, striatum in BG, cerebellum
Late onset Alzheimer’s
Chromosome 19 (ApoE/ApoE4) -> failure in Abeta clearance -> gradual increase in Abeta 42
Familial Alzheimer’s
Chromosone 1 (presenilin 2) Chromosome 14 (presenilin 1) Chromosome 21 (APP)
Cause constant production of Abeta 42 (Abeta 43)
Histology of Parkinson’s dz
Lewy bodies in substantia nigra, locus ceruleus, basal nucleus of Meynert, raphe nucleus, cerebral cortex
Histology of Huntington’s chorea
Intranuclear and cytoplasmic inclusions/Huntington protein, striatum, frontal cerebral cortex
Histology of amyotrophic lateral sclerosis
Bunina bodies/SOD1; UMN, LMN, lateral corticospinal tract
Pick’s dz
Cytoplasmic inclusions, Tau+ Pick bodies composed of densely packed neurofilaments; atrophy in frontal or temporal lobe, cholinergic neuronal loss especially in basal nucleus of Meynert
Progressive supranuclear palsy, corticobasal degeneration, frontotemporal dementia
Neurofibrillary tangles/tau
Progeria
LMNA gene normally encodes prelamin A protein. Mutation in LMNA -> production of abnormal form of prelamin A (progerin) -> blebbing and disorganization of nuclear envelope -> impaired signal transduction, nuclear compartmentalization, and gene regulation