8.13.2010

thalamic lesions short

Thalamic Functional Divisions

1. reticular (arousal) intralaminar (nociception)

2. sensory

3. motor

4. limbic

5. higher cognitive function


Four arteries that perfuse thalamus

1. Tuberothalamic (off of pcom)

2. Paramedian ( p1)

3. Inferolaterals (P2)

4. Posterior choroidal (P2)



12%

Tuberothalamic perfuses - reticular, intralaminar, VA, mamillothalamic tract, amygdalofugal pathway


Pathology - fluctuating arousal, impaired learning and memory, autobiographical memory,

"emotional facial paralysis" - volition but asymmetry when laughing crying

Left VL - anomia, acalculia, comprehension impaired, preserved repetition and reading.

Right VL - hemispatial neglect

contralateral clumsiness


***tuberothalamic confined to anterior (sparing VL/MD) - deficits in new learning/apathy

superimposition of temporally unrelated information parallel expression of mental activities - palipsychism


35%

Paramedian artery perfuses - MD, intralaminar nuclei (CL, CM Pf), periventricular, posteriomedial VL, ventro medial pulvinar

Pathology - neuropscyh disturbances in arousal and memory (left right asymmetry, langauge/visual)

hypophonia, perseveration, agitation, aggressive, apathy

bilateral infarct - deep coma, awake unresponsiveness sudden labile affect changes to mania, inappropriate social behaviors, lack of shame, perseveration

dysarthria!!!

utilization behaviors

thalamic dementia - amnestic syndrome cjd

chronotaraxis - prominent disorientation in time

neurological signs - asterixis, vertical gaze paresis, 6th nerve palsies, bilateral internuclear ophthalmoplegia

miosis, light sensitivity.


45%

Inferolateral artery

Pathology - sensory loss, impaired extremity movement, thalamic pain syndrome - no neuropsych

"thalamic hand" of Foix and Hillemand - flexed, pronated, thumb beneath four fingers, spares language

Principal - VP (M,L,I, pc)

thalamic pain Dejerine and Roussy 1906 hypesthesia, hemiparesis, hemiataxia

Medial branches - (MGN)

Inferolateral pulvinar - rostral and lateral pulvinar


8%

Posterior choroidal -

Lateral - LGN, LD, LP, inferolateral parts of pulvinar

rare - quadrantanopsia, impaired fast phase of optokinetc response opposite the lesion. contralateral hemibody numbness, mild aphasia

homonymous quadrantanopsia, horizontal sectoranopsia, hemisensory loss, transcortical aphasia, memory


Medial - MGN, posterior parts of CM and CL, pulvinar

pulvinar infarct created - hyperkinetic motor syndrome (ataxia, rubral tremor, dysotnia, myoclonus, chorea "jerky dystonic unsteady hand"



Recovery

prognosis is correlated w/volume of hematoma

LOC @ onset

motor weakness @ onset

presence of intraventricular extension/hydrocephalus

generally considered good when consider mortality, recovery of motor

cognitive/psychiatric persistence reported (rates not well established)


Diaschisis - a lesion in one brain region produces impairment in distant but connected region








8.08.2010

Master Neuro exam for adult




Scharfy's Master Neuro Exam for Adults

General Medical

HEENT - otoscope

CV

Resp

Abd

Extremities

Mental Status
 Alert & Oriented to person, place, and time. 

Language

spont. speech

comprehension

naming

repetition

reading

writing

Memory

immediate (telephone number said backwards)

short (3 object recall)

long (presidents)

Calculations

Construction (clock@4:10)
 Abstraction (similarities/differences/aphorism)

Cranial Nerves
CNI

CNII- pupil reaction, acuity, confrontation, funduscope
abnormal - anisocoria is an efferent defect
swing test for afferent pupil defect (marcus gunn)
CNIII, IV, VI - EOMi, look for nystagmus here,
brainstem lesion - "nuclear" gaze palsy no doll's eyes
cortical lesion - "supranuclear" only voluntary is affected, still have doll's eyes
INO - intranuclear ophthalmoplegia
CNV - touch, pin, muscles of mastication
CN VII - close eyes tight, wrinkle forehead
lesion? peripheral vs. central
CN VIII - finger rub
hearing loss -
one ear - has to be peripheral
both ears affected equally - central lesion
CN IX/X - palatal elevation "open up and say ah"
CN IX,X,XI - dysarthria - kuh lah mah
pseudobulbar palsy - bilateral central lesions induce bulbar lesion (dramatic speech/swallow problems) -strained strangled character
bulbar palsy - lower motor neuron lesion (breathy hoarse, hypernasal)
CN XI - scm/shoulder shrug
Trapezius - input from contralateral hemisphere
SCM - input from bilateral hemispheres (mostly ipsi though) Left SCM rotates head to right
CN XII - stick out tongue

Motor System - 0-5
Bulk - note for atrophy/fasciculations
Tone (residual tension) -
spasticity
rigidity
paratonia - tone decreases when patient distracted

Shoulder abduction C5, INT/EXT rotation
Elbow ext C6,7/flex C5,6
Wrist ext C6,7/flex C7,8
Finger flex C8/ext C8 ABD/ADD - T1
Hip flex L2,3/ext L4,5
Knee flex L5S1 /ext L3,4
Ankle dorsi L4,5/plantarflexion S1,2

-paresis - weakness
-plegia -paralyis
-hemi - one side
-para - both lower extremities
-quad - all four extremities

Remember
Central lesion (UMN pattern of weakness)
Upper extremities - flexors stronger than extensors (accounts for pronator drift)
Lower extremities - extensors stronger than flexors

Reflexes (0-4)
brachioradialis
biceps
triceps
patellar
achilles
ankle jerk clonus
plantar response

having troubles?
upper extremity - patient clench teeth
lower extremity - patient hook flexed fingers (Jendrassik)

Sensation
Light touch
L/R/simultaneous (check for extinguishing)
Pain/Temp
only have to choose one
Position (thumbs, big toes)
Vibration

Other
Stereognosis
Graphesthesia
2 point discrimination


Coordination
Finger/toe tapping
Rapid alternating
FNF
Orbiting
Heel to shin
Pronator Drift - drift suggests UMN lesion affecting that arm
Gait
walk, heels, tiptoes, tandem
festination - steps get progressively smaller and gait accelerates
Romberg


Look out for the whole time:
Tremor
Myoclonus
Chorea
Athetosis
Ballismus
Tics
Dystonia

Neurology clinical notes

Dawson's fingers - periventricular plaques visualized on T2 MRI, diagnostic of the autoimmune central nervous system demyelinating disorder known as multiple sclerosis.


Uhthoff's phenomenon - characteristic heat intolerance described by MS patients who report exacerbations of symptoms when core body temperatures increases. Thought to be a result of decreased nerve conduction in the setting of heat stress and pre-existing plaques already impeding nerve conduction. Although first observed in 1890 by German neuro-0phthalmolagist Wilhem Uhthoff, it wasn't supported by electrophysiological data until 2004. MS patients with spinal cord lesions/brainstems tend to have poorer prognoses. Treatment with interferons (beta) decrease relapse by 1/3. Tysabri decreased by 2/3 but associated w/PML after ~18 doses, CD4 count less than 500
treatment of MS in pregnancy overview: 0-3 months do nothing, 3+months consider steroids, try to ride it out w/o treatment if possible. pregnancy can have protective effects by virtue of mom's hormone profile (^^progesterone/estrogens), postpartum can create lots of exacerbations when hormone profile decreases. Marijuana (synthetic controlled doses) has been found to be successful in decreasing MS associated muscle spasm and dolor in controlled trials. Smoking marijuana has a vast case report history of treating pain associated w/MS.

Don't forget to ask about handedness.

Aphasia is a disturbance in language that does not result from impaired motor function (thats dysarthria). There are six dimensions:
1. Spontaneous speech
2. Comprehension
3. Naming
4. Repetition
5. Reading
6. Writing

Although upper motor neurons are classically associated w/hyperreflexia and increased tone, an acute stroke with have a period of flaccid paralysis and and tone will begin to increase.

Admission note includes:
CC
HPI
PMH
Past Surg/Med
Allerg
Social History
Fam History
ROS
Exam
Labs
Imaging
Impression w/differential
Plan (either system or problem based)

Frontal lobe lesion clue: cant saccade contralaterally, ipsilateral gaze deviation
Posterior lesion clue: gaze deviates contralaterally

Medical stroke work up:
MRI/MRA
ASA 325mg
Stating 80mg (no matter the lipid profile they do better with them)
TTE/TEE

Acute steroid side effects to watch out for:
Gastritis (give Nexium)
Hyperglycemia (insulin sliding scale)
Hip osteonecrosis
Catacracts/glaucoma
Immunosuppression

stroke 3rd leading cause of death in US, 780K a year, 150K die a year. $60 billion annual cost.

Hemorrhagic strokes #1 cause HTN - normally rupture in deep structures and subcortical branches-
50% of the time: Putamen (pure motor stroke)
50% of the time: either caudate, thalamus, pons, cerebellum

>65 years old -amyloid angiopathy commonly lobar strokes

dosen't fit above? think tumor/abscess/vascular malform

Ischemic strokes - 80% of strokes
can be caused by htn - think deep structures
atherosclerotic strokes
large vessel can have embolus
artery to artery
cardioembolic
dissection
artery to artery embolus
progressive occlusion
full thickness rupture b/c intracranial vessels have thinner media and do not have external elastic lamina.

can be sudden/spontaneous
sudden neck trauma
fibromuscular dysplasia
substance abuse
hypercoaguable states
cancer
heme cancer
genetic (antiphospholipid, factor V etc..., homocysteine, vasculitides)
vasculitides
infxn, autoimmune, endovascular lymphoma
#1 CNS vascular pathology - granulomatous angiitis

"depression can influence recovery"

ACEi/ARBs not as good in African American populations for controlling BP, better to use diuretics or Ca++ channel blocker

advice from site director during clinic, "learn at least one personal thing about each patient and you will be ahead of the game"
"surgery is an option of last resort"



Epilepsy driving laws - need to be 1 year seizure free, doctor does not have duty to report to DMV,

infections also cause cardioembolic stroke - bacterial endocarditis

"DVT prophylaxis starts w/fondaparinux then start heparin in a few days"

Key to neurology - where's the lesion? should be able to get the answer if you take a careful history.

Person having ischemic stroke, allow them to autohypertense - don't treat BP until > 220/110 only need one pressure to exceed. If you are planning to give tPA, the cutoff is reduced to 185/110.

Post stroke HTN normally decreases in 48 hours by self, 4-5 days patient returns to pre-ischemic pressures. Restart antihypertensives ~72 hours after.

Types of neglect:
spatial neglect - looks only to one side, doesn't even know other side of visual field exist have them draw the face of clock
auditory neglect- wont hear you if your voice coming from neglected side (very strange phenomenon)
tactile neglect
visual neglect