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159 Cards in this Set
- Front
- Back
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What is the triad of symptoms for Horner's syndrome? What causes this syndrome?
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Ptosis, anhidrosis, miosis. Lesion of the spinal cord above T1 -- strongly associated with Pancoast tumor.
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Where are the chain sympathetics located?
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T1 to L3.
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What cell type forms multinucleated giant cells in the CNS in response to HIV infection?
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Microglia.
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What cell type acts as the macrophage of the CNS?
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Microglia.
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A tumor of this cell type will have an elevated GFAP is called a glioblastoma multiforme.
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Astrocyte.
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What cell type undergoes reactive gliosis in response to injury in the CNS?
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Astrocyte.
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Each one of these cells myelinates multiple CNS axons.
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Oligodendrocytes (oligodendroglia).
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Other than oligodendroglia, what other cells exhibit perinuclear cytoplasmic clearing ("fried egg" appearance)?
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Koilocytes (due to HPV infection); testicular seminoma cells.
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These cells are destroyed in multiple sclerosis.
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Oligodendroglia.
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What are the CNS/PNS derivatives of neural ectoderm?
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CNS neurons, ependymal cells (line ventricles, make CSF), astrocytes, oligodendroglia.
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What are the CNS/PNS derivatives of neural crest?
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Schwann cells and PNS neurons.
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What are the CNS/PNS derivatives of mesoderm?
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Microglia (like macrophages, they originate from mesoderm).
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This cell myelinates only one PNS axon and is destroyed in Guillain-Barre syndrome.
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Schwann cell.
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What is the origin of an acoustic neuroma affecting CN VIII and located in the internal acoustic meatus?
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Schwann cell. It's a schwannoma.
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Which two molecules are elevated in neural tube defects?
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AFP and acetylcholinesterase in the CSF.
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What is the adult derivative of the telencephalon?
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Cerebral hemispheres.
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What is the adult derivative of the diencephalon?
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Thalamus.
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What is the adult derivative of the mesencephalon?
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Midbrain.
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What is the adult derivative of the metencephalon?
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Pons, cerebellum.
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What is the adult derivative of the myelencephalon?
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Medulla.
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What lab abnormality might point you to a diagnosis of anencephaly?
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Elevated AFP, elevated acetylcholinesterase, polyhydramnios.
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Describe the Chiari II malformation and how it presents.
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Posterior fossa malformation. Tonsillar herniation through the foramen magnum. Acqueductal stenosis and hydrocephaly. Syringomyelia, thoraco-lumbar myelomeningocele.
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What are the two posterior fossa malformations?
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Chiari II and Dandy-Walker.
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How does syringomyelia present?
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Compression of the STT at C8-T1 causes "cape-like", bilateral loss of pain and temperature sensation in upper extremities.
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What are the components of the blood-brain-barrier?
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Tight junctions between nonfenestrated capillary endothelial cells, basement membrane, astrocyte foot processes.
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What disorder is thought to arise from an increase in NE activity? How about a decrease in NE activity?
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Anxiety; depression.
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What disorder is thought to arise from an increase in dopamine activity? How about a decrease in dopamine activity?
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Schizophrenia; Parkinson's.
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Where is 5-HT synthesized?
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Raphe nucleus.
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In which neurological diseases is ACh altered?
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Decreased ACh in Huntington's. and Alzheimer's (due to destruction of the basal nucleus of Meynert).
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What is the main inhibitory neurotransmitter of the CNS? In which diseases are levels altered?
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GABA; decreased in anxiety, Huntington's.
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Which nucleus of the hypothalamus makes ADH? Which makes oxytocin?
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Supraoptic; Paraventricular.
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Which nucleus of the hypothalamus is responsible for the circadian rhythm?
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Suprachiasmatic.
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Which nucleus of the hypothalamus controls the parasympathetic NS? What happens when it is stimulated? Inhibited?
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Anterior/preoptic; sweating and cutaneous vasodilation in hot climates (i.e., cooling off); lesion here = hyperthermia.
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Which nucleus of the hypothalamus regulates the sympathetic NS? What happens when it is stimulated? Inhibited?
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Posterior; shivering and decreased cutaneous blood flow in cold climates (i.e., heating up); lesion here = hypothermia.
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Which area of the hypothalamus is responsible for hunger? What happens if there is a lesion here? Who inhibits this area?
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Lateral; lesion here = anorexia and failure to thrive. Inhibited by leptin.
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Which area of the hypothalamus is responsible for satiety? What happens if there is a lesion here? Who inhibits this area?
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Ventromedial; lesion here = hyperphagia, obesity, savage behavior!; Stimulated by leptin.
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Which area of the hypothalamus is responsible for hunger? What happens if there is a lesion here? Who inhibits this area?
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Lateral; lesion here = anorexia and failure to thrive. Inhibited by leptin.
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Which nucleus of the hypothalamus is involved in the release of GnRH?
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Anterior/preoptic.
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Which area of the hypothalamus is responsible for satiety? What happens if there is a lesion here? Who inhibits this area?
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Ventromedial; lesion here = hyperphagia, obesity, savage behavior!; Stimulated by leptin.
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What is the embryological origin of the posterior pituitary (neurohypophysis)?
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Neural ectoderm.
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Which nucleus of the hypothalamus is involved in the release of GnRH?
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Anterior/preoptic.
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What EEG wave forms correspond to the different stages of sleep?
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Awake/Alert: Beta waves
Awake, eyes closed: Alpha waves Stage 1 (light sleep): Theta waves Stage 2: Sleep spindles and K complexes Stage 3: Delta (slow) waves Stage 4: Delta (slow) waves REM: Beta waves |
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What is the embryological origin of the posterior pituitary (neurohypophysis)?
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Neural ectoderm.
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In which stage of sleep does the normal person spend the most time?
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Stage 2.
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What EEG wave forms correspond to the different stages of sleep?
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Awake/Alert: Beta waves
Awake, eyes closed: Alpha waves Stage 1 (light sleep): Theta waves Stage 2: Sleep spindles and K complexes Stage 3: Delta (slow) waves Stage 4: Delta (slow) waves REM: Beta waves |
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In which stage does the deepest, non-REM sleep occur?
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Stage 3.
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In which stage of sleep does the normal person spend the most time?
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Stage 2.
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What is the "key" to initiating sleep?
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Serotonin production by the raphe nucleus.
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In which stage does the deepest, non-REM sleep occur?
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Stage 3.
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What is the principal neurotransmitter involved in REM?
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ACh.
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What is the "key" to initiating sleep?
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Serotonin production by the raphe nucleus.
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Extraocular movements during REM are due to the activity of what structure?
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PPRF.
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What is the principal neurotransmitter involved in REM?
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ACh.
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Extraocular movements during REM are due to the activity of what structure?
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PPRF.
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During which stage of sleep does sleep terror disorder occur?
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Stage 3/4.
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What is the pathway by which retinal information induces the release of melatonin?
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retina senses darkness --> SCN --> NE release --> pineal gland --> melatonin.
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In which sleep disorder does cataplexy occur?
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Narcolepsy.
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Describe the sleep pattern of a depressed patient.
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Decreased REM latency; early REM; increased total REM.
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Describe the embryological origin of the branchial cleft (groove), arch, and pouch.
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Ectoderm; Mesoderm; Endoderm.
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What is the derivative of the first branchial cleft?
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External auditory meatus.
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Which cranial nerves innervate the branchial arches?
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V (v2 and v3), VII, IX, X.
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What structures are derived from the 1st branchial arch? Abnormalities?
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Meckel's cartilage, mandible, muscles of mastication (temporalis, masseter, lateral and medial pterygoids), mylohyoid, anterior belly of digastric, tensor tympani, tensor veli palatini, anterior two-thirds of tongue; CNs V2 and V3; failure of neural crest to migrate = mandibular hypoplasia, facial abnormalities.
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What structures are derived from the 2nd branchial arch?
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Reichert's cartilage: stapes, styloid, stylohyoid; muscles of facial expression, stapedius, stylohyoid; innervation by CN VII.
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What structures are derived from the 3rd branchial arch? Abnormalities?
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Stylopharyngeus; CN IX innervates (swallowing!). Congenital pharyngocutaneous fistula d/t persistence of cleft pouch --> cleft in lateral neck, aka BRANCHIAL CYST.
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What structures are derived from the 4th-6th branchial arches?
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Thyroid and cricoid cartilage; 4th = pharyngeal constrictors (cricothyroid, levator veli palatini); CN X (superior laryngeal branch -- SWALLOW). 6th = muscles of larynx; CN X (recurrent laryngeal branch - SPEAK). Both contribute to posterior one-third of tongue.
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What are the derivatives of the first branchial pouch?
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Middle ear cavity, eustachian tube, mastoid air cells.
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What are the derivatives of the second branchial pouch?
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Epithelial lining of the palatine tonsil.
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What are the derivatives of the third branchial pouch?
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Inferior parathyroids, thymus.
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What are the derivatives of the fourth branchial pouch?
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SUPERIOR parathyroids.
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What causes DiGeorge syndrome?
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Aberrant development of the 3rd and 4th branchial pouches --> immune cell deficiency (thymic aplasia) and hypocalcemia (failure of parathyroid development).
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Which cranial nerves have their nuclei in the medulla?
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CNs IX, X, XI, XII
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Which cranial nerves have their nuclei in the pons?
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CNs V, VI, VII, VIII
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Which cranial nerves have their nuclei in the midbrain?
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CNs III, IV
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What information is communicated at the nucleus solitarius?
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Visceral SENSORY information from CNs VII (taste), IX (baroreceptors), X (gut distention).
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What information is communicated at the nucleus ambiguous?
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Motor innervation of pharynx, larynx, and upper esophagus via CNs IX, X, XI
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What information is communicated at the dorsal motor nucleus?
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Autonomic (parasympathetic) fibers to heart, lungs, upper GI.
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Which CNs pass through the cavernous sinus?
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CNs III, IV, V1, V2, VI
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What causes cavernous sinus syndrome and how does it present?
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Mass effect (tumor, bacterial infection-induced thrombosis, etc); opthalmoplegia, opthalmic and maxillary sensory loss.
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What gene defect is responsible for DiGeorge syndrome?
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Deletion on chromosome 22q11.
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Lower extremity deficit in sensation or movement may indicate involvement of which artery? What about a deficit in upper extremity movement or sensation?
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Anterior Cerebral Artery.
Middle Cerebral Artery. |
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What cortices do the following arteries supply: ACA, MCA, PCA?
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ACA: Anteromedial surface.
MCA: Lateral surface. PCA: Occipital and inferior surfaces. |
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Where is the lesion in Kluver-Bucy syndrome? What are the sx? What bug is it associated with?
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Amygdala.
Hyperorality. Hypersexuality. Disinhibition. HSV-1. |
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Where is the lesion in spatial neglect syndrome?
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Non-dominant parietal lobe (typically the R).
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Where is the lesion in Gerstmann syndrome? What are the sx?
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Dominant parietal lobe (typically the L). Sx include acalculia, agraphia, finger agnosia, L-R disorientation.
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Where is the lesion that is responsible for alterations in arousal and wakefulness?
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Reticular activating system (midbrain).
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Where is the lesion in a patient with Wernicke-Korsakoff syndrome? What typically is the cause of this lesion?
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Mammillary bodies. Thiamine deficiency.
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A lesion to the basal ganglia results in what?
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Tremor at rest, chorea, athetosis (e.g. Parkinson's).
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A lesion to the cerebellar hemisphere leads to what sx?
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Intention tremor, limb ataxia. IPSILATERAL DEFECTS!
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A lesion to the cerebellar vermis results in what sx?
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Truncal ataxia, dysarthria.
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What area is lesioned in a contralateral hemiballismus?
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Subthalamic nucleus.
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Anterograde amnesia is the result of a lesion to what area of the brain?
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Hippocampus.
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A lesion to the PPRF causes what sx?
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Eyes look away from the side of the lesion.
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A lesion to the superior colliculi produces what ocular sx?
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Paralysis of upward gaze.
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Poor vocal expression suggest a lesion in what area of the brain? What about poor comprehension? Poor repetition?
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Broca's. Wernicke's. Arcuate nucleus. Arcuate fasciculus.
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What is the most feared consequence of carotid artery occlusion?
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Ruptured plaque leading to an embolic stroke!
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What artery supplies the medial lemniscus and medullary pyramid of the medulla?
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Anterior spinal artery.
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Where does the CST decussate in the brainstem? Where does the DCML pathway decussate?
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Medullary pyramids. Medulla.
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What is the path of the STT?
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Peripheral neurons --> DRG --> ascend 1-2 vertebral levels via Lissauer's tract --> decussation to the other side of the spinal cord via the anterior white commissure --> VPL of thalamus --> primary somatosensory cortex.
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What diseases might have Bell's palsy as a complication?
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"My Lovely Bella Had An STD": Lyme disease, Herpes zoster, AIDS, Sarcoidosis, Tumors, Diabetes.
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What should you immediately think of in a patient with "bilateral Bell's palsy"?
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Guillain-Barrè syndrome.
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A patient has a leftward deviation of the tongue on protrusion and has a right-sided spastic paralysis. Where is the lesion?
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Left CNXII nucleus (medulla).
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If the right vagus nerve or nuclei is damaged, to which side will the uvula deviate?
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Uvula will deviate to the left.
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If the portion of the R motor cortex that innervates the soft palate is damaged, to which side will the uvula deviate?
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Uvula will deviate to the right.
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A patient comes to your office and upon saying "Ah" you see the uvula deviate to the left. What neurological areas might be damaged in order for the abnormality to occur?
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Right vagal nerve (CN X), Right nucleus ambiguus, Left corticobulbar tract, soft palate portion of the left motor cortex.
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If the right hypoglossal nerve or nuclei is damaged, then to which side will the tongue deviate when sticking out?
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The tongue will deviate to the right.
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If the portion of the right motor cortex that innervates the tongue is damaged, to which side will the tongue deviate?
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The tongue will deviate to the left.
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How do the sx of a lesion to the cortical motor region of the face differ from a lesion of the facial nerve or nucleus?
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Lesion in the cortical motor face region = paralysis of the contralateral side of the lower face.
Lesion of the facial nerve or nucleus = Ipsilateral paralysis of ENTIRE face. |
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What vessel is occluded in lateral medullary syndrome (Wallenberg syndrome)? What are the sx?
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PICA. Loss of pain and temperature sensation over contralateral body, loss of pain and temperature sensation over ipsilateral face, hoarseness, dysphagia, loss of gag reflex (all d/t damage of nucleus ambiguus), ipsilateral Horner's syndrome (descending sympathetics), vertigo, nystagmus, N/V (vestibular nuclei), ipsilateral cerebellar defects (ICP damage).
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Lesions of the nucleus ambiguus are specific to which artery?
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PICA.
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Lesion to what artery causes medial medullary syndrome? What are the sx?
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Anterior Spinal Artery. Contralateral paralysis (CST damage), contralateral tactile and kinesthetic defects (ML damage), tongue deviates toward side of lesion (CN XII damage). PRESERVATION OF PAIN & TEMP SENSATION.
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What causes Weber syndrome? What are the symptoms?
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Lesion to PCA. Sx include CN III palsy (ipsilateral ptosis, lateral strabismus, pupillary dilation), contralateral hemiparesis.
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What is the cause of medial inferior pontine syndrome? What are the sx?
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Occlusion of the Basilar Artery. Contralateral spastic hemiparesis (damage to CST), contralateral loss of light touch/vibration/kinesthetic sensation (damage to ML), paralysis of gaze toward side of lesion (damage to PPRF and CN VI), ipsilateral paralysis of LR muscle (damage to CN VI). PAIN AND TEMP INTACT.
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Facial nucleus effects are specific to lesion of which artery?
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AICA.
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Occlusion of AICA causes what syndrome? What are the sx?
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Lateral pontine syndrome. Vomiting, vertigo, nystagmus (damage to vestibular nuclei), paralysis of face, decreased lacrimation, salivation, decreased taste from anterior 2/3 of tongue, decreased corneal reflex, decreased pain and temp sensation from face, ipsilateral hearing loss, ipsilateral Horner's syndrome (Damage to nuclei of CN VII, CV V, CN VIII, and sympathetic fibers).
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A patient cannot abduct her left eye on lateral gaze and convergence is normal. She is also having difficulty smiling. In what part of the CNS is there a lesion?
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Pons (CN V, VI, VII, VIII).
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What is the clinical presentation of a patient with internuclear ophthalmoplegia (MLF syndrome)? Causes?
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Difficulty with LATERAL GAZE. Nystagmus in abducting eye. MEDIAL RECTUS PALSY in adducting eye. In patients <50 yrs suspect MS, in patients >50 yrs suspect stroke.
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A lesion of what artery can cause "locked in" syndrome?
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Basilar.
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What is the most common site for a berry aneurysm? What type of hemorrhage occurs if this ruptures?
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Anterior communicating artery. Subarachnoid hemorrhage.
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What are some risk factors for berry aneurysms?
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ADPCKD, Ehlers-Danlos, Marfan's syndrome, AV malformation, advanced age, HTN, smoking, race (African-Americans have increased incidence).
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What are the features of an epidural hematoma? What vessel(s) is ruptured?
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Often secondary to fracture of TEMPORAL BONE, LUCID INTERVAL, rapid expansion under systemic arterial pressure --> trantentorial herniation. CT shows "biconvex disk"/"LENS" not crossing suture lines. Rupture of MIDDLE MENINGEAL ARTERIES. Often involves the temporal lobe. BLOWN PUPIL (CN III).
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What vessel is ruptured in a subdural hematoma? What are the features of this IC hemorrhage?
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BRIDGING VEINS. CT scan shows CRESENTIC SHAPED hemorrhage that crosses suture lines. MIDLINE SHIFT.
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Who is at risk of developing a subdural hematoma?
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Elderly, Alcoholics, Blunt trauma victims, shaken babies.
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What is the most common cause of a subarachnoid hemorrhage? What are the sx? What will you see on spinal tap? Tx?
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Ruptured berry aneurysm. "Worst headache of my life". Bloody or yellow (xanthochromic) spinal tap. Tx with nimodipine.
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What is the most common cause of intraparenchymal hemorrhage? What part of the CNS does this occur in?
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Systemic HTN. Basal ganglia and internal capsule.
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Who is vulnerable to interventricular hemorrhage?
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Premature infants (younger than 30-32 weeks) and very LBW infants --> within 72 hours of delivery.
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You have an ischemic brain event. At what point will you see neutrophils and necrosis? Macrocytes? Reactive gliosis? Scarring?
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24-72h the PMNs show up. Macrocytes show up 3-5d after event. Reactive gliosis at 1-2 wks and glial scarring after 2 weeks.
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Outline the venous drainage of the brain.
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Cerebral veins --> venous sinuses --> internal jugular vein.
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What is the path of CSF flow through the CNS?
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CSF is synth by the choroid plexus in the lateral ventricles --> Foramen of Monroe --> 3rd ventricle --> Cerebral aqueduct --> 4th ventricle --> Foramen of Luschka (lateral subarachnoid space), Foramen of Magendie (medial subarachnoid space) --> superior sagittal sinus --> arachnoid granulations. Done.
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What clinical features characterize normal pressure hydrocephalus? Reversible or not?
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"Wet, Wobbly, Wacky": Urinary incontinence, ataxia, dementia. REVERSIBLE CAUSE OF DEMENTIA IN THE ELDERLY!
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What is the difference between communicating and noncommunicating hydrocephalus?
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Communicating = Decreased CSF reabsorption at arachnoid villi.
Noncommunicating = Blockage of CSF flow. |
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What are the characteristic features of pseudotumor cerebri and who gets this?
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Unexplained increase in ICP in a obese female with morning headaches that get better throughout the day, pulsating tinnitus, +/- N/V, diplopia, retro-ocular pain, absence of ventricular dilation on CT, NO TUMOR OR MASS.
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What is the most worrisome sequelae of pseudotumor cerebri? What might cause it? Tx?
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VISION LOSS. Long-term tetracylcine use, OCPs, Excessive Vitamin A. Tx includes removing offending agent, lose weight, ACETAZOLAMIDE.
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Which nerve roots are tested in the various clinical reflexes?
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Ankle: S1, 2
Knee: L3, 4 Biceps: C5, 6 Triceps: C7, 8 |
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What are the differences between the 1a and 1b afferent motor pathway?
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1a afferent motor --> causes contraction of muscle (excitatory) so your arm doesn't get ripped off when you try to pick up a heavy suitcase.
1b --> causes relaxation of muscle (inhibitory) so you can release the heavy suitcase before it snaps your muscle. |
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What portion of the thalamus relays somatosensory information from the body? Cerebellum and basal ganglia? Trigeminothalamic and taste pathways to somatosensory cortex?
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VPL; Ventral lateral; VPM.
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What portion of the thalamus relays information from the retina to the occipital lobe? Basal ganglia to prefrontal, premotor, and orbital cortices? Auditory info from IC to primary auditory cortex?
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Lateral geniculate; Ventral anterior; Medial geniculate.
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Where do the fibers of the lateral CST decussate? Where is the first synapse? What disease can affect this tract and where?
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Medullary pyramids; Cell body of the anterior horn; Polio, West Nile virus, and ALS affect the anterior horn.
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What are the classic signs of an UMN lesion? LMN lesion?
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UMN: Hyperreflexia, spastic paralysis, + Babinski, increased tone, clasp knife reflex.
LMN: Hyporeflexia, flaccid paralysis, fasciculations, atrophy, decreased tone. |
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What is the difference b/w essential tremor, resting tremor, and intention tremor?
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Essential tremor is often familial in origin and occurs at rest and with movement. Resting tremor is characteristic of Parkinson's disease and disappears with voluntary movement. Intention tremor is indicative of cerebellar damage and appears with voluntary movement.
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What are the sx associated with anterior lobe (anterior vermis) syndrome? What is the most common cause?
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This region belongs to the legs, so with damage you get ataxia/dystaxia of the legs. Commonly caused by chronic alcoholism, B1 deficiency, degeneration of cerebellar cortex.
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Motor control on which side of the body would be affected with a lesion on one side of the cerebellar hemisphere?
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Motor control ipsilateral to the side of the lesion would be affected. This is because the cerebellum sends information to the contralateral thalamus --> cortex --> CST --> body CONTRALATERAL to cortex.
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What structure provides the major output pathway from the cerebellum?
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SCP --> contralateral VL thalamus.
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Describe the general flow of information through the cerebellum.
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Mossy and climbing fiber inputs --> cerebellar cortex --> Purkinje fiber --> deep nuclei of cerebellum --> output targets.
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What portion of the CNS is affected in Parkinson's? What are the sx? What is the surgical treatment?
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Substantia nigra pars compact is destroyed w/ loss of dopaminergic neurons --> depigmentation. Sx include resting tremor, cogwheel rigidity, akinesia, and postural instability. Lesion the subthalamic nuclei (normally it inhibits movement).
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What is the inhibitory nt of the CNS? Excitatory?
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GABA. Glutamate.
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Lewy bodies are associated with what disease?
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Parkinson's.
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What causes hemiballismus?
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Lesion of the contralateral subthalamic nuclei = no stimulation of the globus pallidus interna = no inhibition of the thalamus.
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Which Parkinson's drug(s) is used to agonize dopamine receptors?
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Bromocriptine, pramipexole, ropinirole.
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Which Parkinson's drug(s) is used to increase dopamine?
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Amantidine (increased dopamine release) and L-dopa/Carbidopa.
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Which Parkinson's drug(s) is used to prevent the breakdown of dopamine?
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Selegiline (MAO type B inhibitor), entacapone, tolcapone (COMT inhibitors).
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Which Parkinson's drug(s) is used to curb excess cholinergic activity?
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Benztropine (antimuscarinic).
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What toxicities are associated with Levodopa?
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Arrhythmias from peripheral conversion to DA, dyskinesia, akinesia.
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How do the following structures normally impact movement: Globus pallidus internal segment, subthalamic nucleus, substantia nigra pars compacta?
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GPi = inhibits movement.
STN = inhibits movement. SNc = stimulates movement. |
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What nt characteristics are seen in Huntington's disease? Which drugs are used in tx of HD?
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Increased Dopamine and decreased ACh and GABA.
Reserpine and Tetrabenazine --> nuke DA. Haloperidol --> DA receptor antagonist. |
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What are "The C's" of Huntington's disease?
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CAG repeats.
Chorea. Crazy. Chromosome 4. Caudate nuclei. |
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What is the genetic mutation in Friedrich's ataxia? What are the sx? What is the cause of death typically?
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Trinucleotide repeat disorder (GAA) in the gene encoding FRATAXIN. Staggering gait, frequent falling, nystagmus, dysarthria, hammer toes, pes cavus. Presents in childhood with ataxia. Hypertrophic cardiomyopathy is the COD.
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What are the findings of Brown-Sèquard syndrome?
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Ipsilateral loss of DCML, Ipsilateral UMN signs, Contralateral loss of pain and temp sensation, Ipsilateral loss of ALL SENSATION at level of lesion, LMN signs at level of lesion.
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What malformation is associated with syringomyelia?
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Arnold Chiari II or III malformation.
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What clinical presentation would lead you to suspect ALS as a dx?
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Combined UMN and LMN deficits with intact sensation.
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