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109 Cards in this Set
- Front
- Back
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what 3 groups don't return to baseline after traumatic brain injury?
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1. those with previous neurologic damage (concussions are multiplicative), 2. those with psychiatric illness, 3. those involved with litigation
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what are the 5 symptoms of postconcussive syndrome?
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decreased concentration, irritability, disturbed sleep, fatigue, headache
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what is the course of postconcussive syndrome?
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peak at 2 weeks post injury, subsides with 90% return to baseline in 6 months
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what is a serious consequence of second impact syndrome?
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it can trigger cerebral edema leading to herniation and death
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what are the late effects of a closed traumatic brain injury?
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tearing of bridging veins secondary to force
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in what populations should we worry about shearing of bridging veins?
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elderly and young and alcoholics - more space between skull and brain
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a pt with a concussion slowly develops more neurologic deficits in the days after the initial injury. What should we worry about?
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tearing of the bridging veins that caused a subdural hematoma
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how is memory regained?
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backwards forward and forward backwards
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what is diaschisis?
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shock waves of injury due to high velocity impact from a penetrating missile wound
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what are the 3 late sequelae of penetrating head injury?
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1. CNS infection, 2. hydrocephalus, 3. seizures (focal not generalized)
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what are the signs of hydrocephalus?
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wet, wacky, wobbly - gait instability, incontience and change in mental status
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which lobes are most sensitive to anoxia?
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temporal lobes = decreased memory and ability to learn
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what occurs secondary to hypoxia?
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hydrocephalus ex. Vacuo
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what are the 3 mechanisms of damage in acquired brain injury?
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anoxia, hypoxia and toxic-metabolic exposure
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what is the mechanism of damage in hypoxic brain injuries?
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ischemia and edema (hypercarbia, inflammatory response)
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what are the late effects of hypoxia?
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persisting memory deficits (dementia), seizure due to scarring and gliosis and parkinsonian signs - due to sensitivity of the BG to hypoxia
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what type of seizure would be likely due to injury to the temporal lobe?
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complex partial seizures (mesial temporal sclerosis)
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what is a typical episode of complex partial seizures?
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aura - feeling like you are in an elevator, an unpleasant smell etc. followed by loss of awareness and memory and maneristic behavior - picking, hand washing etc. with no memory of the episode
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what is the primary mecahnism of damage of peripheral nerves?
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axon compression
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what is the most common focal neuropathy?
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carpal tunnel syndrome
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what causes carpal tunnel syndrome?
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entrapment of the median nerve beneath the flexor retinaculum at the wrist, prolonged pressure leads to ischemia
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symptoms: numbness, tingling pain in the wrist and first 3.5 fingers
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carpal tunnel syndrome
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which muscle is wasted in carpal tunnel syndrome?
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adductor pollis brevis
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which muscles are spared in carpal tunnel syndrome?
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first dorsal interosseous and /adductor digiti minimi
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which disease can positive tinel and phanel signs?
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carpal tunnel syndrome
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what type of etiology causes carpal tunnel in diabetics?
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increased nerve susceptibility to pressure injury
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what type of diseases cause reduced space in the carpal tunnel leading to carpal tunnel syndrome?
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RA, ganglia, gouty tophi and palmar infection
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what causes ulnar neuropathy?
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repetitive nerve compression against bone, but can result from elbow "tardy ulnar palsy"
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what disease causes: numbness over the dorsal and palmar aspects of the last 1.5 fingers?
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ulnar neuropathy
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what muscles are affected with ulnar neuropathy?
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FDI and ADM but NOT APB
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what diseaes give postitive froment's sign and ulnar claw hand?
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ulnar neuropathy
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what disease gives tinel's sign at the elbow?
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ulnar neuropathy
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what is the mechanism of damage in radial neuropathy?
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most commonly compressed radial nervea gainst the humerus in the region of the spiral groove
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what disease gives you wrist drop?
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radial neuropathy
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what disease gives you numbness over the 'snuff box'?
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radial neuropathy
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what muscles are affected in radial neuropathy?
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weakness of finger and wrist extensors, but triceps usually spared = can differentiate neuropathy from stroke
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symptoms: abrupt numbness/burning over middle/lateral thigh
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meralgia paresthetica
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are there muscle weakness or decreased knee reflex in meralgia paresthetica?
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no, there is no weakness and normal knee jerk
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what is the treatment of meralgia paresthetica?
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none, it usually resolves spontaneously
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what are the 2 causes of polyneuropathy (generalized peripheral nerve disorder)?
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1. axonal, 2. demyelinating
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what clinical features suggests polyneuropathy?
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sensory AND motor symptoms that involve both upper and lower extremities - stocking and glove pattern that occurs gradually has has decreased deep tendon reflexes
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which symptom is greater in axonal loss polyneuropathy?
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sensory > motor
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which symptom is greater in demyelinating polyneuropathy?
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moter > sensory
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what are the clinical features of length dependent axonal polyneuropathy?
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1. numbness, tingling, pain that is constant, 2. worse at night, 3. involves legs then arms, 4. sensation disturbance before distal muscle weakness 5. impotence, orthostatic hypotension, 6. occasional exacerbation - touch, cold, wind etc
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how do you treat axonal polyneuropathies?
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treat underlying disease, minimize foot/hand injuries, treat symptoms
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what is the major etiology of axonal polyneuropathy?
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diabetes!! Can be caused by alcoholism, gout, hypothyroidism, and other systemic disorders
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how do you differentiate between polyneuropathy and multiple mononeuropathies?
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1. patchy symptoms in mono (poly is symmetrical feet then hands), 2. in mono there is a step wise acquisition of deficits of the individual nerves
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when would you suspect inherited polyneuropathy?
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1. if the patient is < 50yoa, 2. especially with a family history, 3. high arched feet, hammer toes, 4. marked distal atrophy "stick man", 4. "inverted champange bottle" legs, 5. MR, tremor, multiple systems involved
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what are the symptoms of demyelinating polyneuropathy?
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early weakness, areflexia and sensory ataxia due to disruption of large fiber nerve function
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what are the 3 features of acquired demyelination?
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1. parital motor conduction block, 2. temporal dispersion, 3. asymmetric conduciton slowing between nerves and in poximal/distal segments of the same nerves
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what is the most common mechanism of damage of segmental demyelinating polyneuropathies?
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usually immune mediated
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what is guillain barre syndrome?
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segmental demyelinating polyneuropathy
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what are the symptoms of guillain barre?
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symmetrical mild pain/tingling (sensory), progressive ascending weakness of legs and arms that occurs over a few days. Eventually slurred speech with facial weakness; absent reflexes
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what 3 groups of cell are affected by amyotrophic lateral sclerosis?
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anterior horn cells (LMN), motor nuclei of the brainstem (LMN), pyramidal cells of the motor cortex (UMN)
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what are the symptoms of ALS?
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slowly progressive (4-6 months) weakness, fatigue and muscle wasting and muscle twitching that starts in one extremity eventually there is dysphagia and SOB
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what happens to reflexes in ALS?
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they are increased!!
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what happens to the tongue in ALS?
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there are tongue fasciculations and atrophy
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what are the results of a nerve conduction study on the sensory nerves of an ALS patient?
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sensory nerves are normal, it is the motor nerves that have low amplitutude response, but the conduction velocites are normal
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what populations are affected by MG?
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young (20-30s) - women; and elderly (60-70s) - men
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what is the most common primary neuromuscular disorder?
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MG
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what is the most common presentation of MG?
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diplopia and droopy eyelids (ptosis), difficulty chewing, swallowing or talking and limb weakness (less common)
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what is the hallmark of MG?
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fatigable weakness
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what test can be done if you suspect MG?
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tensilon (edrophonium - short acting AChE inhibitor) test
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How does MG affect sensation, reflexes, coordination and gait?
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MG doesn't, they are all normal
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symptom: patient complains of heaviness and numbness in one limb
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myopathy
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which muscles, distal or proximal, are more affected by myopathy?
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proximal = hard to climb stairs, get up from low seats, lift arm above head etc
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what happens to cranial nerves, sensation, reflexes, coordination in myopathy?
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they should be normal
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what will the CK levels be for myopathy in systemic disease, inflammatory myopathy and muscular dystrophy?
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low CK in myopathy in systemic disease; in between CK in muscular dystrophy; high CK in inflammatory myopathy
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what is a very common systemic cause of muscle disease?
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steroid myopathy - especially in COPD patients
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what does the muscle biopsy show in muscular dystrophies?
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muscle fiber degernation, regeneration, proliferation of endomysial CT (fibrosis) and replacement of muscle tisue with fat; any inflammation is SECONDARY
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what is the inheritance pattern of Duchene and Becker MD?
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X-linked recessive
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how are Duchenne and Becker MD different?
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in duchenne there is complete absense of dystrophin, becker it is decreaed. Duchenne onset is <5, becker >5 yoa; MR is common with Duchenne and it is the more severe disease
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what does it mean if a patient's muscle biopsy shows a central core?
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they have a tendency to develop malignant hyperthermia during anesthesia
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what population is affected by inclusion body myositis?
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> 50 yoa, male
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histology: muscle with rimmed vacuoles, neurogenic atrophy, inflammatory cell infiltration (sometimes) and amyloid deposition
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inclusion body myositis
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does inclusion body myositis respond well to steroids?
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no
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what is the presentation of inclusion body myositis?
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similar to dermatomyositis and polymyositis but involves incidious onset of weakness in the distal muscles, especially extensors of the knee and flexors of the wrists and finger. It is more asymmetrical than the other two
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muscle histology: ragged red fibers and subsacrolemmal accumulations that are reactive for succinate dehydrogenase
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mitochondrial disease
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CNS histology: multiple strokes of different ages, neuronal loss, mineralized neurons and reactive gliosis
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mitochondrial disease
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what are 3 featurs of mitochondrial disease?
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1. ragged red fibers due to accumulation of abnormal mitochondria, 2. drop out fibers, 3. abnormal mitochondria - crystalloids, abnormal shape
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what causes McArdle disease?
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point mutation on 11q that causes a deficiency of myophosphorylase; A is <10% of normal, B is greatly elevated
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what are the symptoms of McArdle disease?
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muscle symptoms only - easily fatiguable, muscle cramps, myoglobinuria, wasting and weakness of proximal muscles in later disease
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what does the CK look like in McArdle disease?
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consistently elevated
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histology: necrotic and regenerating fibers, subsarcolemmal vacuoles, excessive glycogen storage, abnormal polysaccharide storage (can't be digested by diastase) and negative for phophorylase reaction
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McArdle disease
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histology: centrally located pale core on NADH-TR reaction
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central core myopathy
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histology: presence of nemaline bodies
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nemaline body myopathy
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histology: smal type 1 fibers, normal sized type 2 fibers
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X-linked myotubular myopathy
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histology: centrally located nuclei in all fibers
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central nuclear myopathy
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what happens to muscle fibers in X-linked myotubular myopathy?
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the muscle fibers fail to mature
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what population is affected by X-linked myotubular myopathy?
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neonatal
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what are the manifestations of X-linked myotubular myopathy?
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severe hypotonia and weakness EXCEPT IN EXTRAOCULAR MUSCLES, respiratory paralysis and dysphagia
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what muscles are not affecting in X-linked myotubular myopathy?
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extraocular muscles
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what is the genetics of X-linked myotubular myopathy?
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X-linked recessive, mutation on MTM1 gene that codes for myotubulin
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when does MS initally present?
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around 30 yoa, female:male 2:1
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CSF: oligoclonal IgG bands
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MS
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CSF: moderate mononuclear pleocytosis and slight increase in protein level, increased IgG
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MS
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what is the most sensitive method to detect MS?
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MRI - periventricular plaques that are ovoid with long axis parallel to the ventricles, enhancement is seen in acute but not chronic plaques
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gross: almond to oval lesions in the white matter
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MS
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Histology: perivascular chronic inflammation with loss of myelin, often multiple lesions at different stages
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MS
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Is reactive gliosis or inflammation more porminent in chronic plaques?
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in chronic plaques reactive gliosis is more prominent, in acute plaues inflammation is more prominent
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an acute multifocal inflammatory and demyelinating disease that is often associated with a preceding infectious agent
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acute disseminated encephalomyelittis
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symptoms: acute onset of somnolence, confusion and often convulsion, can progress to coma
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acute disseminated encephalomyelittis
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gross: swelling and edema of the brain but no other macroscopic changes
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acute disseminated encephalomyelittis
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histology: multifocal perivenous lymphocytic infiltration that extends into surrounding parenchyma; demyelination with blood vessels at epicenter
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acute disseminated encephalomyelittis
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non-inflammatory acute demylinating diseaes that affects the pons and is associated with alcoholics (Wernicke-Korsakoff or hyponatremia)
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central pontine myelinolysis
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diseaes that is associated with rapid over correction of hyponatremia in alcoholics
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central pontine myelinolysis
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presentation: rapid evolving spastic paraparesis with pseudobulbar palsy, changes in mental status with confusion and coma; "locked in" syndrome is typical
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central pontine myelinolysis
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gross: upper pons has butterfly or triangular shpaed symmetrical midline lesion of demyelination rimmed by areas of preserved myelination
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central pontine myelinolysis
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histology: axonal swelling, with transverse (pontocerebellar) fibers more affected than rostral cuadal fibers (corticospinal or corticobulbar)
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central pontine myelinolysis
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