Neuro Lesions Flashcards

1
Q

In brainstem lesions, damage to long tract results in a

A

contralateral deficit

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2
Q

In brainstem lesions, damage to CN results in a

A

ipsilateral deficit

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3
Q

___ signs inform you of brainstem level in brainstem lesions

A

CN signs

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4
Q

Characteristics of SPINAL CORD LESIONS involving LONG TRACTS

A
  1. effects observed at level of lesion and below
  2. pain and temp loss side opposite of lesion
  3. weakness, position sense and vibration sense lost ipsilaterally
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5
Q

medial medullary lesion

A

Reticular Formation
-respiration, BP, HR

Medial Lemniscus
-position, vibration loss (contralateral)

Corticospinal Tract
- hemiparesis (contralateral)

CN XII: Hypoglossal

  • ipsilateral tongue paralysis
  • fasiculations
  • protrusion causes tongue deviation TWD lesion
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6
Q

lesion to nucleus gracilis or nucleus cuneatus –> (ipsilateral/contralateral) damage

A

lesion to nucleus gracilis or nucleus cuneatus –> IPSILATERAL damage

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7
Q

hypoglossal lesion (medulla)

A
  • paralysis of tongue ipsilaterally
  • fasciculations (LMN) ipsilaterally
  • upon protrusion, tongue deviates to side of lesion
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8
Q

nucleus ambiguus lesion (medulla)

A
  • hoarseness
  • difficulty swallowing
  • ipsilateral droop of arch of soft palate
  • contralateral uvula deviation
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9
Q

spinal nucleus of V (medulla)

A

ipsilateral deficit pain/temp from face

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10
Q

damage to inferior cerebellar peduncle may result in ____ on the side of the lesion

A

damage to inferior cerebellar peduncle may result in ATAXIA on the side of the lesion

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11
Q

Lateral medullary lesions causing damage to certain fibers that originate in the hypothalamus can result in ___________ syndrome

A

Horner’s syndrome

damage to fibers that originate in the hypothalamus and descend to the spinal cord to control sympathetic NS to ipsilateral face

ptosis, miosis, anhidrosis

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12
Q

paralysis of LOWER face tells you right away that you have a lesion of the

A

in contralateral corticobulbar pathway (UMN)

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13
Q

paralysis of WHOLE side of face indicates which type of lesion?

A

ipsilateral lesion of facial nucleus or nerve (LMN)

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14
Q

lesion to vestibulo-ocular system (pons)

A

eyes shift toward lesioned side (contralateral vestibular input dominates)

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15
Q

lesion to cochlear nucleus (pons)

A
  • difficulty localizing sound

- difficulty eliminating background noise

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16
Q

medial pontine syndrome

A
  • contralateral loss of position/vibration sense in body (ML) - may be partial
  • contralateral hemiparesis of body (CST)
  • ipsilateral paralysis of lateral rectus m. (VI) –> diplopia on lateral gaze
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17
Q

lateral pontine syndrome

A
  • contralateral loss of pain/temp in body (STT)
  • ipsilateral loss of pain/temp in face (spinal V)
  • ipsilateral facial paralysis (VII)
  • deafness (VIII)
  • ipsilateral loss of facial sensation, paralysis of m. of mastication (V)
  • ipsilateral ataxia (middle cerebellar peduncle)
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18
Q

lesion of MLF (medial longitudinal fasciculus)

A

weakness in medial rectus muscle (adduction) of ipsilateral eye

(internuclear ophthalmoplegia)

often caused by MS

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19
Q

lesion of PPRF (Paramedian Pontine Reticular Formation)

A

inability to gaze toward weakened side

(horizontal gaze palsy)

PPRF sends impulses DIRECTLY to abducens (lateral rectus)
and across pons to MLF to III (medial rectus)

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20
Q

disease of which structure would affect vertical eye movements?

A

diseases of the midbrain

vertical gaze is controlled by Rostral Interstitial Nucleus of MLF, which sits just behind the red nucleus (midbrain)

^ often disrupted by stroke or tumors of the pineal gland

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21
Q

medial midbrain lesion

A

contralateral hemiparesis (CST)

Ipsilateral CN III palsy (pupil dilation, ptosis, weak medial rectus)

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22
Q

somatic motor nuclei of the brainstem (III, IV, VI, XII) are all located _____ (involved in _____ brainstem lesions)

A

somatic motor nuclei of the brainstem (III, IV, VI, XII) are all located MEDIAL (involved in MEDIAL brainstem lesions)

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23
Q

branchial motor nuclei of the brainstem (motor V, facial VII, ambiguus IX/X, spinal accessory XI)) are all located _____ (involved in _____ brainstem lesions)

A

branchial motor nuclei of the brainstem (motor V, facial VII, ambiguus IX/X, spinal accessory XI)) are all located LATERAL (involved in LATERAL brainstem lesions)

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24
Q

lateral medullary lesion

A

SST
- pain/temp loss bod (contralateral)

descending V
- pain/temp loss face (ipsilateral)

ambiguus

  • hoarseness
  • uvula deviation (contralateral)

inferior cerebellar peduncle
- ataxia (ipsilateral)

descending sympathetics
- Horner’s (ipsilateral)

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25
Q

medial midbrain syndrome

A

contralateral hemiparesis (CST)

ipsilateral CN III palsy (pupillary enlargement, ptosis, oculomotor palsy)
- fixed, wide pupil pointed down and out

26
Q

which lesions causes pupillary enlargement, ptosis, and oculomotor palsy?

A

medial midbrain syndrome

ipsilateral CN III palsy

27
Q

Acoustic neuroma

vestibular schwannoma

A
  • tumor coming off VIII near cerebellopontine angle (OUTSIDE brainstem)
  • often vestibular signs first, then cochlear
    (ringing –> deafness) ipsilateral
  • later V and VII involvement (face numbness, m. weakness) ipsilateral
  • even later, pons can get squished: long-tract involvement (ataxia via middle cerebellar peduncle, hemiparesis via CST)
28
Q

basilar a. occlusion

A
  • bilateral hemiparesis (both CST)
  • bilateral sensory loss (ascending systems)
  • variable CN signs
  • reticular system (BP, respiration)
    involved –> coma
    spared –> “locked-in syndrome”
29
Q

vascular disease (stroke, etc.) time course

A

minutes-hours

30
Q

enlarging mass (tumors, etc) time course

A

days-weeks

31
Q

degenerative diseases (MS, etc) time course

A

months-years

32
Q

sx are occurring over minutes-hours, suspect…

A

vascular disease (stroke, etc.)

33
Q

sx are occurring over days-weeks, suspect…

A

enlarging masses (tumor)

34
Q

sx are occurring over months-years, suspect…

A

degenerative diseases (MS, etc)

35
Q

pseudobulbar palsy

A

looks like brainstem disease, is not

bilateral CBT lesions (ALS, bilateral strokes, MS)

bilateral CN palsies

release of brainstem reflexes for emotional responses (inappropriate laughing/crying)

36
Q

CN lesion + limb weakness, ataxia or sensory sx

where is lesion?

A

inside brainstem

37
Q

multiple CN signs w/o long tract signs

where is lesion?

A

subarachnoid space

38
Q

multiple, contiguous, unilateral CN signs

where is the lesion?

A

skull base (right where CN exit) or cavernous sinus

39
Q

isolated CN lesion

A

uncertain but more likely peripheral location

40
Q

See III, IV, V (V1, V2), VI signs ipsilaterally, suspect lesion is where?

A

cavernous sinus

41
Q

See V, VII, VIII signs ipsilaterally, suspect lesion where?

A

cerebellar-pontine angle

42
Q

See IX, X, XI, XII signs ipsilaterally, suspect lesion where?

A

skull base

43
Q

lesions of the cerebellum lead to deficits contralateral or ipsilateral to lesion?

A

ipsilateral to lesion

44
Q

lesion to flocculonodular lobule

A

balance and gait ataxia
oculomotor control –> nystagmus

(vestibulocerebellum damage)

isolated syndrome rarely seen in humans

45
Q

vermal and paravermal degeneration

A

truncal/leg incoordination

(spinocerebellar and olivary input)

common w/ alcoholism and malnutrition

46
Q

neocerebellum

A

upper extremity dyscoordination

neocerebellum damage, receiving corticocerebellar input

47
Q

sx of cerebellar disease

A

incoordination - ataxia

dysmetria

intention tremor

dysdiadochokinesis

nystagmus

hypotonia

48
Q

acute cerebellar disease

A

cerebellar hemorrhages and infarcts

toxic exposure

  • mercury poisoning (Minamata disease)
  • toluene (glue sniffing)
  • med toxicity

heat stroke

anoxia

49
Q

subacute cerebellar disease

A

alcoholism –> vermal damage

paraneoplastic syndrome –> anti-Purkinje Abs (anti-Yo)

post-infectious cerebellar ataxia

cerebellar tumors

MS

50
Q

chronic cerebellar disease

A

congenital cerebellar hypoplasia

genetic disorders (spinocerebellar ataxia)

neurodegenerative (olivopontocerebellar degeneration (mult systems atrophy))

51
Q

dysdiadochokinesis

A

speed of movement initiation reduced; tested by performing rapidly alternating movements

seen w/ lesion of cerebellar hemispheres

52
Q

dysmetria

A

overshooting or undershooting movements due to inability to control limb acceleration and deceleration

seen w/ lesion of cerebellar hemispheres

53
Q

four cardinal features of hypokinetic disorders

A

“Parkinsonism”

1) BRADYKINESIA (required)
2) resting tremor
3) rigidity
4) postural instability

54
Q

symptoms of hyperkinetic disorders

A
  • tremors (rhythmic, oscillatory)
  • hemiballismus (violent, flailing)
  • myoclonus (rapid, jerk like)
  • chorea (random, purposeless)
  • dystonia (abnormal co-contraction of muscles)
  • tics (stereotypic movements, supressible)
55
Q

Parkinson’s affects which basal ganglia pathway?

A

DIRECT PATHWAY

  • less dopamine is available to activate the direct pathway
  • leads to a NET DEACTIVATION of the cortex
56
Q

features of Parkinson’s disease

A

2+ symptoms:

  • bradykinesia (required)
  • resting tremor
  • rigidity
  • postural instability (late finding)

Asymmetry of symptoms
Functional neuroimaging

57
Q

clinical features of Huntington’s

A

Movement disorder

  • chorea
  • Parkinsonism (late/juvenile cases)

Dementia

Psychiatric

  • depression
  • psychosis
58
Q

pathology of Huntington’s disease

A

Neuronal loss and gliosis in striatum –> atrophy

  • early disease: shift to direct pathway causes chorea
  • late disease: both pathways involved causes Parkinsonism

Neuronal loss in cortex
-cognitive and psychiatric symptoms

59
Q

neuronal loss and gliosis in striatum causes

A

neuronal loss and gliosis in striatum causes ATROPHY

60
Q

disruptions in basal ganglia physiology causing dopamine deficient state can lead to which disorders?

A

hypokinetic disorders

61
Q

disruptions in basal ganglia physiology causing an increase in dopaminergic or thalamic activity can lead to which disorders?

A

hyperkinetic disorders