Neuro 4 Flashcards

1
Q

Describe difference in presentation of UMN vs. LMN disorder in the face

A

UMN disorder = weakness of lower face with sparing of upper face

LMN disorder = weakness of upper and lower face

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2
Q

Describe the different levels (e.g. muscle, nerve, etc.) that can cause weakness

A

Muscle, NMJ, peripheral nerve, nerve root, plexus, spinal cord, cerebral hemisphere/brainstem

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3
Q

Describe pattern of weakness in primary muscle disorders

A

• Symmetric proximal muscle weakness that can affect neck muscles

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4
Q

Associated signs and sx in primary muscle disorder

A
  • Muscle pain if inflammatory

* Should not cause sensory or reflex deficits

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5
Q

Pattern of weakness in NMJ disorder

A
  • Wekness of proximal muscles
  • Some characteristically affect extraocular and bulbar muscles
  • Fluctuation in degree of weakness (may change hour to hour)
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6
Q

Associated signs and sx of NMJ disorder

A

• Should not show sensory signs or sx

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7
Q

Pattern of weakness in peripheral nerve disorder

A
  • Mononeuropathy = weakness in muscles innervated by a single peripheral nerve
  • Polyneuropathy = dysfunction occurs first in the muscles of the distal extremities symmetrically
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8
Q

Associated signs and sx of peripheral nerve disorder

A

• May cause numbness, tingling, or pain

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9
Q

What does radiculopathy mean?

A

• Radiculopathy = problem involving a single nerve rooth

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10
Q

Pattern of weakness in nerve root disorder

A

• Causes weakness in the muscles innervated predominantly by fibers from one nerve root

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11
Q

Associated signs and sx of nerve root disorder

A
  • Radiating pain and tingling are common

* If the nerve root serves a particular muscle stretch reflex, that reflex may be depressed or absent (e.g. C5 = biceps)

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12
Q

Pattern of weakness in plexus disorder

A

• Multiple muscles in a limb are weak and do not conform to a particular nerve root or peripheral nerve pattern

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13
Q

Associated signs and sx in plexus disorder

A

• Associated sensory signs of reflex loss common

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14
Q

Pattern of weakness in spinal cord disorder

A
  • Weakness in a UMN pattern below the lesion (due to interruption of the descending corticospinal tract)
  • Weakness in a nerve root pattern at the level of the lesion (mimics radiculopathy)
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15
Q

Associated signs and sx in spinal cord disorder

A
  • Sensory loss below lesion due to interruption of acending tracts
  • Reflexes below level of lesion are increased and Babinksi usually present
  • Bowel and bladder incontinence may occur
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16
Q

Pattern of weakness in cerebral hemisphere disorder

A
  • Weakness of the contralateral side in an UMN pattern
  • Parasagittal lesions lead primarily to leg weakness
  • Lateral lesions lead primarily to face and arm weakness
  • Deep lesions may lead to weakness in all 3 parts
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17
Q

Associated signs and sx of cerebral hemisiphere disorder

A
  • L hemispheric lesions may cause aphasia and apraxia
  • R hemispheric lesions may cause neglect or visuospatial dysfunction
  • Brainstem lesions may have accompanying CN findings
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18
Q

Describe typical presentation of tension HA

A

Constant pressure in temporal and occipital region. Band-like pattern. No nausea, vomiting, or photophobia

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19
Q

What is a physical exam finding that remains present in brain dead patients

A

Deep tendon reflexes (spinal cord may still be functioning)

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20
Q

What part of the brain is damaged in alcohol neurotoxicity

A

Cerebellum (specifically the vermis = defect in truncal coordination = wide-based gait and postural instability)

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21
Q

Effects of thiamine deficiency in alcohols

A

Werknicke’s triad = confusion, ophthalmoplegia, ataxia

22
Q

Approved medication used in ALS

A

Riluzole = glutamate inhibitor

23
Q

How do you diagnose MS?

A
  • Oligoclonal bands in CSF

- MRI brain shows periventricular hyperintense white matter lesions

24
Q

Tx of MS flair

A

IV glucocorticoids (e.g. methylprednisolone)

25
Q

What is Friedreich ataxia: imaging findings + presentation

A

♣ Autosomal recessive trinucleotide repeat disorder GAA
♣ Degeneration of cerebellum and spinal cord
• Ataxia, muscle weakness (usually arms > legs), loss of vibratory sense and proprioception, diabetes mellitus, hypertrophic cardiomyopathy
• Presents in childood with kyphoscoliosis

26
Q

Classic presentation of CJD

A

Rapidly progressive dementia, myoclonus, and sharp triphasic synchronous discharges on EEG

27
Q

Describe features of vestibular neuritis

A

♣ Acute unilateral peripheral vestibulopathy (not really inflammation)
♣ Features:
• Sudden onset single episode that can last days
• Associated with nausea and vomiting
• Severe vertigo but no hearing loss

28
Q

Describe features of labyrinth concussion

A

Sudden onset vertigo as a result of head injury

29
Q

Describe Meniere disease

A

♣ Increased pressure and volume of endolymph
♣ Features:
• Episodic vertigo with nausea and vomiting
• Ear fullness/pain
• Unilateral sensorineural hearing loss
• Tinnitus

30
Q

Describe perilymph fistula vertigo

A

♣ Results from disruption of the lining of the endolymphatic system
♣ Patients hear a “pop” at the time of sudden increase in middle ear pressure (sneezing, nose-blowing, coughing, straining) followed by abrupt onset of vertigo

31
Q

Describe benign paroxysmal positional vertigo (BPPV)

A

♣ Results from freely moving crystals of calcium carbonate within one of the semicircular canals
♣ Features:
• Brief episodes brought on by head movement
• No auditory symptoms

32
Q

Describe typical sx associated with peripheral vs. central vertigo

A

Peripheral = tinnitus and hearing loss

Central = diplopia, dysarthria, and other sx of brainstem dysfunction

33
Q

What are the signs and sx of cerebellar diseas

A

Dysmetria, intention tremor, dysdiadochokinesia, gait ataxia, truncal ataxia, dysarthria, nystagus

34
Q

What is dysmetria

A
  • Abnormlaity of the range of force of a movement

* Erratic, jerky movmements with over-and undershootin the target

35
Q

What is dysdiadochokinesia

A

• Abnormality of the rate and rhythm of a movement demonstrated by asking the patient to perform a rapid alternating movement

36
Q

Paraneoplastic cerebellar degeneration is usually associated with what cancers?

A

Gynecologic or small cell lung cancer

37
Q

Diagnose: sudden onset cerebellar ataxia with associated vomiting and depressed level of arousal

A

Cerebellar stroke

38
Q

What disease other than Marfan’s presents with a Marfanoid habitus?

A

Homocystinuria

39
Q

Difference in presentation between Marfan syndrome and Homocystinuria

A

Marfan:

  • Marfanoid habitus (pectus deformity, tall stature, arachnodactyly, joint hyperlaxity, skin hyperelasticity, scoliosis)
  • **Normal intellect
  • Aortic root dilation
  • Upward lens dislocation

Homocystinuria:

  • Marfanoid habitus
  • **Intellectual disability
  • Thrombosis (Homocysteine is prothrombotic, which may lead to premature acute coronary syndrome)
  • Downward lens dislocation
  • Megaloblastic anemia
  • **Fair complexion
40
Q

Most common infectious cause of single brain abscess

A

Usually direct extension from an adjacent tissue infection

Strep Viridans, Staph aureus

41
Q

Describe presentation of Neurofibromatosis type 1

A

♣ Neurocutaneous disorder characterized by café-au-lait spots, cutaneous neurofibromas (peripheral nerve sheath tumors), optic gliomas, pheochromocytomas, Lisch nodules (pigmented iris hamartomas)
♣ Neurofibromas consist of proliferation of Schwann cells, fibroblasts, and neurites
• Appear as soft, nontender, pedunculated cutaneous lesions

42
Q

Describe presentation of neurofibromatosis type 2

A
♣	Bilateral acoustic schwannomas, juvenile cataracts, meningiomas, and ependymomas
♣	Presentation:
•	Hearing loss, tinnitus, balance problems, hyperpigmented skin lesions, cataracts 
♣	REMEMBER 2’s:
•	Chr 22
•	Bilateral hearing loss
•	NF Type 2
•	Cataracts
43
Q

Presentation of acute closure glaucoma

A

♣ Rapid onset severe eye pain
♣ May see halos around lights
♣ Affected eye will appear injected with dilated pupil that is poorly responsive to light
♣ Can also have tearing and HA with subsequent nausea and vomiting

44
Q

DIfferentiate between Cauda equina syndrome and Conus medularis syndrome

A

• Cauda equina syndrome
o Likely due to disc herniation or rupture, spinal stenosis, tumors, infection, hemorrhage, or iatrogenic injury
o Causes LMN signs as the nerve roots are part of the peripheral nervous system
o Usually bilateral, severe radicular pain
o Saddle hypo/anesthesia
o Asymmetric motor weakness
o Hyporeflexia/areflexia
o Late-onset bowel and bladder dysfunction

•	Conus medullaris syndrome
o	Causes both UMN and LMN symptoms
o	Sudden onset severe back pain
o	Perianal hypo/anesthesia
o	Symmetric motor weakness
o	Hyperrreflexia
o	Early-onset bowel or bladder dysfunction
45
Q

Describe details of paralysis in Guillan Barre vs. tick-borne

A

• Tick-borne paralysis
o Rapidly progressive ascending paralysis over hours to days
o Paralysis may be asymmetrical

• Guillain Barre syndrome
o Ascending symmetrical paralysis over days to weeks

46
Q

Other sx besides paralysis in Guillan Barre vs. tick-borne paralysis

A

• Tick-borne paralysis
o Absence of fever and sensory abnormalities, and normal CSF

• Guillain Barre syndrome
o Sensation is usually normal to midly abnormal
o Autonomic dysfuction (e..g tachycardia, urinary retention, and arrhythmias) occur in 70% of patients
o CSF is usually abnormal and may show high protein with few cells

47
Q

Tx of tick-borne paralysis vs Guillain Barre

A

Tick-borne = removal of tick resutlt in spontaneous improvement in most patients

GBS = IV Ig or plasmapharesis

48
Q

Describe presentation of Essential tremor

A

♣ Occurs at rest and with movement
♣ Usually genetic
♣ Hands > arms > head&raquo_space; legs

49
Q

Tx of essential tremor

A
  • Beta-blockers
  • Primidone (barbiturate/anticonvulsant)
  • Self-medicated with alcohol
  • Benzodiasepines (clonazepam)
50
Q

Treatment of trigeminal neuralgia

A

Carbamazepine (anticonvulsant)