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OS9.2 - Neuro > Coma, MN Disease, Radiculopathy > Flashcards

Coma, MN Disease, Radiculopathy Flashcards

1
Q

Familial Muscular Atrophy

A

anterior horn cell disease

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2
Q

Poliomyelitis

A

anterior horn cell disease - infection by polio virus

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3
Q

Amyotrophic Lateral Sclerosis

A
  • Upper +/- Lower motor neuron degeneration
  • progressive and lethal within about 5yr (usually)
  • weakness, atrophic fasciculations, hyperreflexia, positive Babinski, spasticity
  • atrophy progresses distal to proximal
  • normal sensation
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4
Q

Werdnig-Hoffmann

A

“Infantile SMA”

  • AR; SMN1/2 on CHR 5q - SMN1 absent, SMN2 short determines infantile type (instead of longer which would be juvenile)
  • progressive LMN disease
  • fatal (usually 2/2 respiratory failure)
  • floppy baby, frog leg posture
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5
Q

Wolfart-Kugelberg-Welander

A

“Juvenile [Proximal Chronic] SMA”

  • AR; SMN1/2 on CHR 5q - SMN1 absent, SMN2 longer determines juvenile (instead of infantile, shorter) type
  • progressive LMN disease
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6
Q

[Progressive] Spinal Muscular Atrophy (SMA)

A
  • progressive LMN disease
  • Infantile (AR): Werdnig-Hoffman
  • Juvenile (AR): Wolfart-Kugelberg-Welander
  • Adult-Onset: sporadic, some are familial
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7
Q

Progressive Bulbar Palsy

A
  • like ALS but primarily affects the muscles innervated by the medulla (“bulbar atrophy”)
  • also tongue atrophy
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8
Q

Progressive Lateral Sclerosis

A
  • only affects UMNs (so like ALS but specific to UMNs)

- sporadic, more benign course (slower progression than ALS)

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9
Q

Differential for ALS

A
  • Multisystem atrophy: late onset degenerative nerve disease that is progressive but slower than ALS
  • Craniocervical junction disorders: get MRI to rule out
  • Cervical spondylosis: would see mostly arm/hand weakness and maybe sensory loss (maybe not); also see on MRI as protruding discs
  • Post-polio syndrome: must have had polio in childhood (cause of this is unknown - age-related degeneration of previously infected LMNs?)
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10
Q

Kennedy Disease

A

“Spinal Bulbar muscular atrophy”

  • caused by androgen receptor mutations (X chr)–DNA test to diagnose
  • classic phenotype = LMN syndrome, gynecomastia, testicular atrophy
  • more benign, may present w/o family history
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11
Q

Non-progressive unilateral limb weakness and atrophy

A
  • a more benign motor neuron syndrome

- etiology unclear but may be caused by dural compression of the spinal cord

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12
Q

How to differentiate ALS from a muscle weakness type presentation of myasthenia gravis or Eaton-Lambert syndrome?

A

Do an EMG.

Also, rule out myopathies with muscle biopsy and serum CPK.

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13
Q

Bunina body

A
  • dense granule inclusions of ubiquitin in cell body cytoplasm of anterior horn cell neurons
  • seen in ALS
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14
Q

Etiology of ALS

A

unknown; some genetic associations include:

  • superoxide dismutase (SOD) mutation (AD, Chr 21)
  • Chr 17-linked FTD
  • others; but all (except SOD mutation) are rare
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15
Q

Treatment of ALS

A
  • there is no cure
  • Glutamate antagonists help
  • symptomatic treatments (anticholinergics, antidepressants, respiratory assistance)
  • PT
  • experimental treatments are out there
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16
Q

2 MCC’s of radiculopathies

A
  1. disc herniation/degeneration (50yo)
17
Q

Clinical Features of Radiculopathies

A

PAIN

  • radiates
  • sharp, hot, stabbing, electric
  • worse when root is stretched (neck extension or straight leg raise maneuvers)
  • pain relieved by walking uphill or riding bike
  • negative sx: weakness, atrophy, paresthesias, diminished or absent sensory loss, muscle stretch reflexes
18
Q

New onset back pain - what could it be?

A
  1. Emergency? - spinal cord compression; cauda equina syndrome; spinal column fracture/dislocation
  2. Bone disease? - OP, OM, Paget, steroids, congenital
  3. Infection? - of the spinal cord is called myelitis; will have fever, pain
  4. Neoplasm? - will often have pain at rest, hx of cancer (if current known cancer consider mets), constitutional sx, neuro deficit (local lesion)
  5. Spinal stenosis? - inc. pain with extension, dec. pain with flexion
19
Q

EDX (electro-diagnostic) testing is used for…

A

assessing nerve fiber function; helps characterize the lesion better than clinical exam

20
Q

Treatment for radiculopathy

A
  • most improve within 6wk
  • keep moving, do PT
  • may use NSAIDs, benzo’s, nerve blocks if severe
  • surgery for structural lesion (don’t do surgery unless there’s a specific known lesion to address)
21
Q

Etiology of most slowly generalized, symmetric, progressive stocking-glove neuropathy

A

Toxic-metabolic:

  1. diabetes
  2. alcohol abuse
22
Q

C6 - innervates which finger?
C7 - innervates which finger?
C8 - innervates which finger?

A

C6 - thumb
C7 - middle finger
C8 - pinky
In between fingers are mixed

23
Q

Etiology of most subacute-onset, generalized, symmetric, weakness with distal sensory abnormalities

A

acquired demyelinating neuropathy

24
Q

Etiology of most chronic generalized, symmetric, stocking-glove distribution weakness, out of proportion to degree of sensory loss

A

hereditary dysmyelination

25
Q

Multiple mononeuropathy - characteristics and etiologies

A
  • asymmetric

- etiologies may be ischemic, inflammatory/immune-mediated; infectious, genetic, mechanical entrapments, neoplastic

26
Q

2nd most common entrapment neuropathy

A

ulnar - numb pinky

or really any nerve that comes from C8

27
Q

Froment’s sign

A
  • in order to grasp something between the thumb and index finger (first dorsal interosseous) the patient must flex the last phalanx of the thumb
  • cheating to hold the paper when you try to pull it away
  • flexing palmaris longus
28
Q

Brain structures that mediate consciousness

Lesions of what areas will cause coma?

A
  • extensive acute bilateral hemispheres
  • lesions of thalamus and hypothalamus
  • periaqueductal gray
  • upper 1/3 of pontine tegmentum
29
Q

How to distinguish structural vs. metabolic coma?

A
  • structural will have focal neuro deficit, abnormality on CT, and may produce herniation; likely requires surgical intervention; pupils are first to go
  • metabolic will have a non-focal exam, normal brain imaging or diffuse changes; medical management; pupils are last to go (will still be sluggish)
30
Q

What treatment is needed immediately for a patient in coma?

A
  1. stabilize vitals - ABCs, cardiac monitoring, IV access
    * it’s unusual to have normal vitals in a true coma
  2. stabilize neck, determine circumstances of onset
  3. rapidly examine the patient
  4. empirical D50, thiamine, naloxone
  5. give O2, control ICP*, stop seizures, tx infxn, restore electrolytes, control agitation
    * hyperventilation will rapidly reduce ICP for ~30min
31
Q

How to prognosticate outcome after coma?

A
  • at presentation: higher the GCS, better the outcome
  • non-traumatic coma at day 3: poor prognosis if no pupillary light/corneal reflex or no/flexor/extensor motor response
  • hypoxic coma: absence of purposeful motor movements at day 3 carries poor prognosis
32
Q 
Lethargic vs.
Hypersomnic vs.
Obtunded vs.
Stuporous vs. 
Coma
A

Lethargic - sleepy but easily aroused
Hypersomnic - excessively sleepy, but normal when awakened
Obtunded - mental blunting, decreased alertness
Stuporous - eyes open briefly after vigorous stimulation, then return to deep sleep; impaired cognition
Coma - eyes remain closed after vigorous stimulation (2-4wk in coma they’ll have eye opening and sleep-wake cycles)

33
Q

Abulia vs.
Akinetic mutism vs.
Minimally conscious state vs.
Vegetative state

A

Abulia - awake but apathetic, no spontaneity
Akinetic mutism - silent, alert-appearing immobility
Minimally conscious state - fragments of awareness
Vegetative state - awake but no awareness or meaningful interaction with the environment

34
Q

Two components of consciousness

A
  1. Arousal: sleep-wake cycles, seated in AAS; disease causes stupor/coma
  2. Content/Awareness: puposeful interaction with the world, these behaviors are premeditated and not reflexive; disease of these cognitive circuits causes dementia
35
Q

How to recognize central herniation at the bedside?

A

Progressive failure of brainstem in rostral direction:
- increasing lethargy 2/2 pressure first on reticular gray in both thalami
- then SNS tracts from hypothalamus –> small pupils
- EW failure –> fixed pupils
- Cheyne-stokes respirations
Late signs:
- decorticate/flexor posturing
- decerebrate/extensor posturing

36
Q

Distinct clinical syndrome of pontine hemorrhage

A
  • abrupt coma
  • pinpoint pupils
  • decerebrate rigidity or flaccid quadriplegia
  • horizontal gaze paresis with vertical ocular bobbing
  • at risk for locked-in syndrome
37
Q

Metabolic encephalopathy

A
  • metabolic insult to the brain causing a non-focal exam with negative CT
  • clues: pupils stay reactive till the end; asterixis*, multifocal myoclonus, and tremor are present
  • MCC in elderly are dehydration, drug intoxication, and infection
  • aka negative myoclonus, a lapse in muscle tone
38
Q

Transition from decorticate to decerebrate posturing

A
  • you are decorticate when you have flexor posturing, because the conscious control of the descending motor tracts (which are flexor-facilitatory) is compromised
  • you progress to decerebrate when the extensor facilitatory tracts that originate in the pons are the only ones left working; that is you lost midbrain and the higher (flexor facilitatory) tracts

OS9.2 - Neuro (10 decks)

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