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
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
Explain the rationale for using immunomodulators for long-term management of relapsing-remitting MS. (SIGS 8.1b)
long-term autoimmune condition that does not have a cure, so manage inflammation and minimize relapses/flare-ups
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
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
Define status epilepticus and discuss nonpharmacologic management of it. (Sigs 8.4a)
seizure that lasts greater/equal to 5 min OR a series of seizures in rapid succession w/o interictal period; airway clear (O2),BP&pulse, EEG
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
Describe the mechanism of action of peginterferon beta-1a in treating MS. (SIGS 8.1b)
supress T cell activity--> decr. proinflammatory cytokines and decr. lymphocyte invasion of CNS
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
Describe the use of nutraceuticals (riboflavin, magnesium, coenzyme Q10) used in the management and prevention of headaches. (Sigs 8.4b)
see image
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 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
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
Distinguish abortive and preventative pharmacotherapies for migraine headache. (SIGS 8.4b)
Prev:Amytriptyline(TCA antidepress-> block reuptake norepi&serotonin),Prochlorperzine(antipsychotic-> block D2r); abort: Ketorolac(NSAID-nonsel), Sumatriptan
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 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)
Discuss the mechanisms of action of the six different drug therapies used to manage PD symptoms. (SIGS 8.2b)
dopamine precursor, decarboxylase inhibitors, dopamine agonists, COMT inhibitors, NMDA antagonists, MAO-B inhibitors, anticholinergic (muscarinic antagonists)
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 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 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
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 clinical presentation and imaging findings of tuberous sclerosis complex (TSC) and relate this to seizures. (Sigs 8.4a)
skin lesions, angiofibromas face, shagreen patches, cafe-au-lait spots, seizure, cardiac myoma; Imaging: hamartomas, giant cell astrocytoma
Discuss the MOA and use of diazepam and levetiracetam for treatment of seizures. (Sigs 8.4a)
D: incr. GABAa action-> calms neuroactivity in brain; L: SV2A receptor blocker-> slows electrical signals in brain