Describe the motor and sensory areas of the cerebral cortex that get their blood supply from the MCA, relating to specific MCA stroke signs/symptoms (Sigs 8.1a)
Motor: broca's area--> expressive aphasia, unilateral motor area--> contralateral hemiparesis; sensory: wernicke's--> receptive aphasia, unilateral sensory area
Describe the RACE score and NIH Stroke Score and how they are used for CVA management. (Sigs 8.1a)
RACE is a pre-hospital assessment to assess possible stroke- EMT; NIHSS is more specific- used by physicians to quantify severity of stroke in acute setting
Describe the vascular and neurogenic migraine hypotheses. (Sigs 8.4b)
V: ischemia due to intracranial vasoconstriction-> aura&rebound vasodilation->perivascular nociceptive activation; N: neuronal hyperactivity occipital cortex
Describe the process of myelination and its role in nerve cell conduction. (SIGS 8.1b)
See image; serves as insulating layer composed of protein and fat that allows electrical impulses to transmit quickly and effectively down nerve axon
Identify mechanisms of demyelination in MS and relate it to possible causes of MS. (SIGS 8.1b)
activation myelin-reactive T cells-> adhesion molecule expression-> enter BBB; antibodies against myelin; inflammation, free radical,& protease release
Explain the rationale for using methylprednisone in an acute MS exacerbation. (SIGS 8.1b)
decr vasodilation & permeability of capillaries + decrease leukocytes + mediate change gene express + inhibit phospholipase A2 & NF-kappa B--> decr. inflam
Describe the role of areas of the brain affected in AD. (SIGS 8.2b)
episodic mem affected 1st; hippocampus (short term mem); cerebellum (procedural mem); hippocampus (new mem encoded); amygdala (emotional mem)
Identify neural pathways affected in AD. (SIGS 8.2b)
memory 1st (hippocampus), then reasoning/language/behavior (frontal &temporal lobes), in later stages motor is affected (motor cortex)
Describe the motor symptoms of PD across the progression of the disease. (SIGS 8.2a)
dysphagia, micrographia, myoclonus, freezing, festination, shuffling short-stepped gait, speech disturbances
Describe the effects of dopamine depletion in PD. (SIGS 8.2a)
pars compacta in substantia nigra not making dopamine-> cannot act to stimulate D1 excitatory pathway-> unable to inhibit GPi-> incr inhibition of thalamus
Identify a physiologic rationale for the declining efficacy of carbidopa-levodopa treatment over time in PD. (SIGS 8.2b)
dependency on exogenous levodopa vs endogenous + disease progression-> dose dependence-> side effects worsen(dyskinesia)--> discontinue
List the advantages and disadvantages of the drug therapies used to manage PD. (SIGS 8.2b)
some drugs can only be used for short periods due to adverse effects; others if used for a long time have increasing undesired effects/ decreased effectiveness
Describe the clinical presentation of vertigo. (SIGS 8.3a)
rotatory spinning or rocking, possible nausea & vomiting; Meniere triad: peripheral vertigo, tinnitus, asymmetric fluctuating sensorineural hearing loss
Discuss the indications for and mechanism of action of the Epley Maneuver in cases of vertigo. (SIGS 8.3a)
Indication: BPPV; MOA: moves lodged calcium crystal(canalith)debris out of semicircular canal into inner ear-->stereocilia can move-->normalize action potential
Describe the clinical presentation of benign paroxysmal positional vertigo (BPPV) and labyrinthitis. (SIGS 8.3a)
BPPV= abnormal sensation of motion elicited by certain provocative positions--> nystagmus; Labyrinthitis: inflamm disorder-> poor balance & hearing
Contrast the mechanisms of action of fingolimod and natalizumab for relapse prevention in MS. (SIGS 8.1b)
F: sphingosine-1-phosphate analog that decreases lymphocyte invasion of CNS; N: antibody against a4-integrin to decrease lymphocyte invasion of CNS
