Test 3 Cerebellum & NeuroExam CC Flashcards
General Signs of Cerebellar lesions (x3)
What is spared?
Common signs of cerebellar lesions
- Uncoordinated movement
- motor learning problems
- asynergistic movements
- No paralysis or muscle weakness
Truncal ataxia reflects damage to? What are other symptoms/signs you might see?
Vestibulocerebellar dysfunction= damage to nodulus and fastigual nucleus
Symptoms: truncal ataxia, tendency to fall (to side, forward or backward), wide based stance, titubation, nystagmus, head tilt (unrelated to lesion side)
titubation= constant head shake/nod or other axial tremor
Titubation- what is it? what causes it?
- Axial/head shake and tremor (the adorable youtube girl. )
- Caused by vestibulocerebellar (midline lesion)
Damage to spinocerebellar structures is usually from? Sx?
Other lesions that are lateral/medial. So, sx usually represent primary lesion?
- What type of cerebellar damage is permanent?
- Cerebellar cortex lesion are represented on which side of the body?
- What type of cerebellar damage is permanent? Damage to cerebellar cortex + NUCLEI. Lesion to just cortex doesn’t cause permanent problems
- Cerebellar cortex lesions result in motor deficits on IPSilateral side
Symptoms of lateral cerebellar lesions (cerebellar cortex)
- decomposition of movement=dyssenergia- lack of coordinated movement
- hypotonia
- Ataxia w/ unsteady gait-LEAN TOWARDS LESION
- Dysmetria (hyper/hypo)
- kinetic/intention tremor
- dysdiadochokinesia- repeated alternating movements
- Rebound phenomenon- muscles don’t adapt to load (push on physician hands and when it’s removed the pt overshoots)
- dysarthria
- nystagmus- abnormal horizontal movements w/ slow conjugate movement AWAY from side of lesion
Dysdiadokinesia
repeated alternating movements seen in pts with cerebellar cortex lesions
Rebound Phenomenon
Inability for antagonistic and agonistic muscles to to adapt to change in load. If patient pushes on physician hand and the physician moves his had, the patients arm will shoot forward
seen in pts with cerebellar cortex lesions
Peduncular nystagmus
- velocity of conjugate movements during nystagmus is the same in both directions
- seen in pts with cerebellar cortex lesions
Why aren’t visceral motor functions reported with cerebellar lesions
- somatic motor dysfunction is sufficient to diagnose
- the high ICP could cause pressure on medulla. This makes differentiation of medullary vs cerebellar deficits difficult.
Inability to walk in tandem
Vestibulocerebellar dysfunction
heel==> toe motion is difficult. Either walk on toes or heels.
When do we know that the cerebellar lesion caused the visceral deficit?
What are examples of visceral deficits caused by cerebellar damage?
- No increased ICP
- visceral response occurs WITH somatomotor tremor
Ex: pupil dilation, flushing, lowered heart rate and blood pressure.
What sx call for detailed cardio vs neuro exam?
Cardio= chest pain, shortness of breath
Neuro= weakness, difficulty speaking
Dysarthria
- what is it
- how to diagnose
- possible causes
Dysarthria
- speech disorder, can’t articulate words
- ordinary conversation
- CN XII (tongue); CN XI, IX (palate); CN VII (lips) or pharyngeal weakness.incoordination
Language abnormalities are called? Two types?
Aphasia= fluent or non fluent
Non-fluent aphasia=
Broca’s aphasia, expressive aphasia
Lesion in inferior frontal gyrus: pars opercularis, pars triangularis
Fluent aphasia=
Receptive aphasia, Wernicke’s aphasia
normal rhythm, articulation, but neologisms (makes up words)
Lesion in dominant supramarginal and angular gyri
What is anosmia- what is it associated with? CN- what can damage it? What is another version of damage to this nerve?
Anosmia= no smell; always with ageusia= no taste
Parosmia- altered/perverted perception of smell
Dysgeusia= abnormal/unappealing sense of taste
CN I- unilateral damage, trauma to skull base in olfactory groove
Scotoma- whats physiological example of this?
- lesion in retina or optic nerve causing a blind spot.
- Blind Spot at Optic disk= physiologic scotoma
Papilledema- what is it? early signs?
Papilledema
- swelling of optic disk from increased ICP
- disappearance of normal cup, disc margins are blurred, arching
Optic atrophy- examples of primary vs Secondary
Optic atrophy
primary- involves optic nerve= tumor, retrobulbar injury, demyelination
Secondary- chronic increased ICP, infarction or syph
Diplopia can be caused by?
Damage to any extraocular muscles= CN III, IV, VI
SIgns of third nerve palsy, causes?
Causes= Pcomm/ICA aneurysm, uncal herniation,
Signs= paralsyis of ipsilateral muscles, no pupillary dilation, ptosis, can’t look up, down or medially
If one eye is pointed HIGHER than the other?
trochlear nerve palsy on OPPOSITE side!
cross-eyed
Abducens palsy
Two reflexes that test trigeminal nerve?
- Corneal reflex: trigeminal= afferent; efferent is facial
- Jaw Jerk: tap on chin causes afferent (trigeminal); efferent is also trigeminal (muscles of mastication)
If the jaw deviates to RIGHT side when closing?
Right trigeminal nerve injury. Opposite side pterygoid muscles is not being equaled anymore
Testing CN VII vs UMN?
Central VII vs Bell’s palsy
CN VIII dysfunction-
What sx are reported with vestibular dysfunction
- Rinne/Weber test for cochlear portion
- Vestibular dysfunction= vertifo, nausea vomiting, balance issues. Water caloric test- warm same
Testing CN XI and X?
Gag reflex=
Afferent= 9, contraction of stylopharyngeus= 10
Vagus nerve damage clinical sx?
- Hoarse voice, nasal sound
- dysarthria- vocal cord weakness
- dysphagia
- Uvula deviation to healthy side
- tachycardia
CN XI signs
can’t shrug against resistance, winged scapula, cant turn head away from weak side
CN XII lesion
tongue deviates to WEAK side on protrusion (uvula deviates to strong side, jaw to weak side)–paralysis to genioglossus
