Neuro Lesions

Question 1

In brainstem lesions, damage to long tract results in a

Answer 1

contralateral deficit

Question 2

In brainstem lesions, damage to CN results in a

Answer 2

ipsilateral deficit

Question 3

___ signs inform you of brainstem level in brainstem lesions

Answer 3

CN signs

Question 4

Characteristics of SPINAL CORD LESIONS involving LONG TRACTS

Answer 4

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

Question 5

medial medullary lesion

Answer 5

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

Question 6

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

Answer 6

lesion to nucleus gracilis or nucleus cuneatus –> IPSILATERAL damage

Question 7

hypoglossal lesion (medulla)

Answer 7

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

Question 8

nucleus ambiguus lesion (medulla)

Answer 8

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

Question 9

spinal nucleus of V (medulla)

Answer 9

ipsilateral deficit pain/temp from face

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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

Question 12

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

Answer 12

in contralateral corticobulbar pathway (UMN)

Question 13

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

Answer 13

ipsilateral lesion of facial nucleus or nerve (LMN)

Question 14

lesion to vestibulo-ocular system (pons)

Answer 14

eyes shift toward lesioned side (contralateral vestibular input dominates)

Question 15

lesion to cochlear nucleus (pons)

Answer 15

• difficulty localizing sound

- difficulty eliminating background noise

Question 16

medial pontine syndrome

Answer 16

• 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

Question 17

lateral pontine syndrome

Answer 17

• 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)

Question 18

lesion of MLF (medial longitudinal fasciculus)

Answer 18

weakness in medial rectus muscle (adduction) of ipsilateral eye

(internuclear ophthalmoplegia)

often caused by MS

Question 19

lesion of PPRF (Paramedian Pontine Reticular Formation)

Answer 19

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)

Question 20

disease of which structure would affect vertical eye movements?

Answer 20

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

Question 21

medial midbrain lesion

Answer 21

contralateral hemiparesis (CST)

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

Question 22

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

Answer 22

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

Question 23

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

Answer 23

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)

Question 24

lateral medullary lesion

Answer 24

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)

Question 25

medial midbrain syndrome

Answer 25

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

Question 26

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

Answer 26

medial midbrain syndrome | ipsilateral CN III palsy

Question 27

Acoustic neuroma | vestibular schwannoma

Answer 27

- 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)

Question 28

basilar a. occlusion

Answer 28

- bilateral hemiparesis (both CST) - bilateral sensory loss (ascending systems) - variable CN signs - reticular system (BP, respiration) involved --> coma spared --> "locked-in syndrome"

Question 29

vascular disease (stroke, etc.) time course

Answer 29

minutes-hours

Question 30

enlarging mass (tumors, etc) time course

Answer 30

days-weeks

Question 31

degenerative diseases (MS, etc) time course

Answer 31

months-years

Question 32

sx are occurring over minutes-hours, suspect...

Answer 32

vascular disease (stroke, etc.)

Question 33

sx are occurring over days-weeks, suspect...

Answer 33

enlarging masses (tumor)

Question 34

sx are occurring over months-years, suspect...

Answer 34

degenerative diseases (MS, etc)

Question 35

pseudobulbar palsy

Answer 35

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)

Question 36

CN lesion + limb weakness, ataxia or sensory sx where is lesion?

Answer 36

inside brainstem

Question 37

multiple CN signs w/o long tract signs where is lesion?

Answer 37

subarachnoid space

Question 38

multiple, contiguous, unilateral CN signs where is the lesion?

Answer 38

skull base (right where CN exit) or cavernous sinus

Question 39

isolated CN lesion

Answer 39

uncertain but more likely peripheral location

Question 40

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

Answer 40

cavernous sinus

Question 41

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

Answer 41

cerebellar-pontine angle

Question 42

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

Answer 42

skull base

Question 43

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

Answer 43

ipsilateral to lesion

Question 44

lesion to flocculonodular lobule

Answer 44

balance and gait ataxia oculomotor control --> nystagmus (vestibulocerebellum damage) isolated syndrome rarely seen in humans

Question 45

vermal and paravermal degeneration

Answer 45

truncal/leg incoordination (spinocerebellar and olivary input) common w/ alcoholism and malnutrition

Question 46

neocerebellum

Answer 46

upper extremity dyscoordination | neocerebellum damage, receiving corticocerebellar input

Question 47

sx of cerebellar disease

Answer 47

incoordination - ataxia dysmetria intention tremor dysdiadochokinesis nystagmus hypotonia

Question 48

acute cerebellar disease

Answer 48

cerebellar hemorrhages and infarcts toxic exposure - mercury poisoning (Minamata disease) - toluene (glue sniffing) - med toxicity heat stroke anoxia

Question 49

subacute cerebellar disease

Answer 49

alcoholism --> vermal damage paraneoplastic syndrome --> anti-Purkinje Abs (anti-Yo) post-infectious cerebellar ataxia cerebellar tumors MS

Question 50

chronic cerebellar disease

Answer 50

congenital cerebellar hypoplasia genetic disorders (spinocerebellar ataxia) neurodegenerative (olivopontocerebellar degeneration (mult systems atrophy))

Question 51

dysdiadochokinesis

Answer 51

speed of movement initiation reduced; tested by performing rapidly alternating movements seen w/ lesion of cerebellar hemispheres

Question 52

dysmetria

Answer 52

overshooting or undershooting movements due to inability to control limb acceleration and deceleration seen w/ lesion of cerebellar hemispheres

Question 53

four cardinal features of hypokinetic disorders

Answer 53

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

Question 54

symptoms of hyperkinetic disorders

Answer 54

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

Question 55

Parkinson's affects which basal ganglia pathway?

Answer 55

DIRECT PATHWAY - less dopamine is available to activate the direct pathway - leads to a NET DEACTIVATION of the cortex

Question 56

features of Parkinson's disease

Answer 56

2+ symptoms: - bradykinesia (required) - resting tremor - rigidity - postural instability (late finding) Asymmetry of symptoms Functional neuroimaging

Question 57

clinical features of Huntington's

Answer 57

Movement disorder - chorea - Parkinsonism (late/juvenile cases) Dementia Psychiatric - depression - psychosis

Question 58

pathology of Huntington's disease

Answer 58

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

Question 59

neuronal loss and gliosis in striatum causes

Answer 59

neuronal loss and gliosis in striatum causes ATROPHY

Question 60

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

Answer 60

hypokinetic disorders

Question 61

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

Answer 61

hyperkinetic disorders