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gray matter
located in cortex of cerebrum, cerebellum, and brain stem
forms cerebral cortx (outermost layer)
overlies sulci and gyri
folds and groves increase surface area
allows for more efficient processing of information
central aspect of spinal cord
components of grey matter
neural cell bodies
axon terminals
dendrites
nerve synapses
grey matter function
recieves infor from white matter
process info for motor and sensation in spinal cord
processing center for personality, intelligence, motor funciton, planning, organization,language processing and processing sensory info
white matter
located in more central aspect of brain
peripheral aspect of spinal cord
ascending and desceding pathways
white matter components and function
primary axons and coated with myelin
conducts, processes, and send nerve signals up and down spinal cord
spinal cord tracts
spinothalamic tract
pain/temp
spinocerebellar tract
light tough
unconscious proprioceptiom
posterior column
proprioception
vibration
spinal cord
ascending pathways relay sensory infp to the brain
first order neuron (primary afferent); extremity → into brain
second order neuron
third order neuron
first order neuron
extends from skin adn runs to dorsal root ganglion into posterior horn of gray matter in sponal cord until point of decussation

second order neuron
carries sensory impulses to subcortical areas in thalamus

third order neurons
carries impulses to cerebral cortex

spinothalamic tract
pain, temp, contralateral
cross over to opposite side of spinal cord occurs within 1-2 vertebral segments
injury causes loss of pain and temperature sensation contralaterally
L sided brain injury→ R sided loss of pain and temp
components of spinothalamic tract
dorsal root ganglion
substantia gelatinosa
dorsal horn of spinal cord
brain stem
thalamus
primary somatosensory cortex
nerve root injury= sam eside sx
injury to spinal cord or brain= contralateral sx

spinothalamic tract injury- syringomyelia
loss of normal flow of CSF (decreased nutrients→ spinal cord starts to die)
trauma
birth defect
spinothalamic tract injury- anterior spinal artery syndrome
infarction
loss of pain and temperature sensation bilaterally BELOW injury
opposite side
vibration ad proception are preserved (posterior column)
bilateral paralysis below level injury
spinothalamic tract injury- thalamic pain syndrome
initial loss of ALL sensation to contralateral side
then pain to contralateral side (body doesnt know how to turn it off)
may seem to be psychological rather than physiologic
posterior column
extends to thamus and to cerebral cortex
cross over at brainstem
effect of injury at spinal cord of posterior column
causes ipsilateral sx
loss of fine touch
proprioception
vibration
posterior column effect with brain injury
contralateral loss of vibration and proprioception
conditions associated with posterior column injury
tabes dorsalis (untreated tertiary syphalis)
pernicious anemia
brown sequard syndrome
severe B12 deficiency
affects posterior column and lateral (motor)column
compromised nerve transmission
paresthesias
loss of vibratory sense (posterior column)
loss of proprioception (posterior column)
spastic paresis and hyperreflexia (lateral- UMN)
brown sequard syndrome
C spine injury due to trauma, stabbing, abscess, or tumors
involves only one side of spinal cord
loss of spinothlamic tract, corticospinal (motor) tract, and posterior column
classic clinical features for brown sequard syndrome
contralateral loss of pain and temperature
ipsilateral hemiparesis
ipsilateral loss of vibration and proprioception
spinocerebellar tract
controls UNCONSCIOUS proprioception
primarily lower limbs and trunk
walking
ipsilateral
how to eval proprioception for spinocerebellar tract
use finger/toe up/down in space
sx of spinocerebellar tract injury
ataxia
dysmetria
paresthesias
impaired coordination
dont know where hand is going in space
conditions associated with spinocerebellar tract inury
brown seqruard syndrome
tabes dorsalis
B12 deficiency
vitmain e def
similar sx to B12 def + hemolytic anemia
friedreich ataxia
friedreich’s ataxia
autosomal recessive d/o that effects chormosome 9
degeneration of spinocerebellar tract, dorsal root ganglia, dorsal column, lateral corticospinal tracts
sx of friedreich’s ataxia
ataxia
loss of proprioception (dorsal)
spastic paralysis (corticospinal tract-UMN)
loss of DTR (afferent pathway
descending pathway
relay motor instruction from the brain
pyramidal tracts
corticobulbar tract
corticalspinal tract
extrapyramidal tracts
2 interconnecting neuron
interconnnecting neurons of descending pathway
1st order neuron
UMN
cerebral cortex and brain stem
soinal cord to anterior gray horn
2nd order neuron
LMN
spinal cord to skeletal muscles
corticospinal tract
control limb and trunk mvmt
motor cortex to medulla
crossover of lateral corticospinal tract at medulla
crossover of anterior corticospinal tract occurs in spinal cord
ends at junction of UMN and LMN
voluntary motor control
corticobulbar tract
motor response for cranial nerves V, VII, IX, X, XI, and XII
control head, neck, amd face mvmt
extrapyramidal tract
located in brainstem
involuntary motor mvmt
muscle tone
balance
posture
modulator of motor response
sx of injury to extrapyramidal tract
hypokinetic
bradykinetic mvmt
loss of pendulaiton with walking
hyperkinetic
athetosis- writhing/twisting motion of the arm
chorea- invol constant small to large mvmts througout the body
myoclonus
tremors and tics
dystonia
UMN injury
spastic apralysis
limited muscle atrophy
NO fasiculations/fibrilations
hyperrefelxia
babinski reflex mya be present- big toe up
LMN injury
flaccid paralysis
sig atrophy
fasiculations ad fibrilations
hyporeflexia
babinski not present
spinal cord disease
amyotrophic lateral sclerosis
tertiary syphilis
guillan barre syndrome
pernicious anemia
poliomyelitis
amyotrophic lateral sclerosis (ALS)
mixed upper and lower motor neuron sx
UMN- corticospinal tracts
LMN- anterior horns and grey matter
progressive neuro sx
medial survival 3-5years for most cases
pulm infections mcc of death
+ CN involvement
ALS s/sx
bulbar involvement (CN IX, X, XI, XII); sometimes V and VII
swallowing
chewing (CN V)
coughing
breathing
talking
vauge sensory complaints
progressice weakness
cognitive complaints
ALS physical exam
drooping of the palate (CN IX and X)\
depressed gag reflex (CN IX asn X)
poolig of saliva in pharynx (CN IX)
weka cough
tongue wasting with contraction and fasiculations
sensation typically preserved
sphincter function usually intact
UMN- spasticty
LMN- weakness, atrophy, and fasiculations
ALS testing
electromyogrphy
acute and chrinic partial denervation with reinnervation
changes in cervical, thoracic, and lumbar region
two spinal regions and bulbar musculature
ALS drooling control
OTC decongestants
aticholinergics
trihexyphenidyl
amitriptyline
atropine
dextiropmorphan/quinidine
tracheostomy
gastrostomy tube
advanced care directives/palliative care consult
tertiary syphilis
can occur anytime after secondary syphilis
2 types of rxn
hyperproliferative gummatous reaction
rapid onset
prompt response to therapy
diffuse inflammation that involves CNS, large arteries
fatal of not treated
s/sx of tertiary syphilis
skin
cutaneous lesions
multinodular lesions
solitary gummas (painless)
mucous memebranes
nodular gummas
leukoplakia
skeletal
destructive boen lesions
periostits
osteitis
arthritis
tertiary syphilis eye sx
gummatous iritis
optic atropy
cranial nerve palsy
tertiary syphilis cardiovascular s/sx
arteritis of large vessel
leads to MI
aortic regurgitation
CHF
aortic aneurysm
asx tertiary syphilis
abnormal CSF findings
+ spinal fluid serology
lymphocutic pleocytosis
increased protein
meningovascular syphilis
headache
irritability
cranial nerve palsies
unequal reflexes
irregular pupil
accomodation intact with poor/absent light reflexes
CVA
CSF similar to asx findings
tertiary syphilis neuro s/sx
sx can occue in any stage of dz
may br preogressive, disabling, and life threatening
tertiary syphilis s/sx general paresis
involvement of cerebral cortex
loss of concentration
memory loss
dysarthria
tremors fingers/lips
irritability
headaches
personality change
slovenly, irresponsible, confused, and psychotic
tertiary syphilis labs
lumbar puncture
indicared if signs of neurosyphilis or ocular involvementn
evidenc eof tx failure
VDRL
RPR
repeat serology testing q3-6months post treatment
tertiary syphylis tx
aqueous PCN
ceftriaxone if PCN allergy
tabes dorsalis
chronic progressive demyelination of posterior columns to posterior roots/ganglia
proprioception
virbration
posterior sensory ganglia
nerve roots
tabes dorsalis s/sx
agryll robertson pupil
poor light reaction
accommodation intact
muscle hypotonia
hyporeflexia
progressive ataxia
wide based gait/inability to wlak in dark
tabes dorsalis PE findings
paresthesias
analgesia
radicular type pain
charcot joints
painless, destructive arthritis with progressive deformity
tabes dorsalis labs
CSF
normal to increased lypmphcytic cell count
elevated protein
guillain barre syndrome causes
can follow illness
a/w camplyobacter jejuni enteritis
undercooked or raw poultry MCC
inoculations
surgery
guillain barre syndrome s/sx
weakness
proximal emphasis
starts in lefs can extend to arms and face
muscles of respiration/deglutition
sensory
distal paresthesias
neuropathic and radicular pain
autonomic sx
tachy
hypo vs hypertension
cardiac irregularities
abnormal sweating
pulm dysfunction → vent + ICu
guillain barre syndrome labs
CSF
increased protein
normal cell count
WBC greater than 50
guillain barre syndrome tx
hospitalization
plasmapheresis
IVIG
respiratory toileting
airway suctioning, chest PT, incentive spirometry, nasotracheal, suctioning
chest pt
DVT prophylaxis bc laying in bed fro long recovery
ICU admission if decreasing forced vital capacity
LONG RECOVERY
pernicious anemia findings
proprioceptive loss
weakness and spaciticy ( UMN sx)
posterior column and corticospinal tract involvement
subacute combine degnereation
impaired B12 absorption due to lack of intrinsic factor
pernicious anemia s/sx
glossitis→ check VitD
anorexia
diarrhea
peripheral nuropathy
balance/proprioception issues (posterior problem)
dementai sx
pale to icteric
loss of vibration
pernicious anemia labs
CBC
moderate to severe megaloblastic anemia
decreased retic count
decreased Vit B12
<200
elevated methylmalonic acid
elevated homocysteine levels
pernicious anemia tx
parental B12
IM vs SubQ
methylcobalamin
oral vs SL
neuro sx
parenteral B12 preferred
poliomyelitis
anterior horn involvement
LMN
weakness
atrophy severe
fasciculation/fibrilations
hyporeflexia
highly contagious
fecal oral route
enterovirus affects anterior horn
polio abortive s/sx
fever
HA
vomiting
diarrhea vs constipation
sore throat
polio nonparalytic s/sx
abortive sx +
meningeal irritaiton
muscle spasms
absence of paraluysis
polio paralytic s/sx
flaccid asymmetric paralysis
proximal muscles lower extremities
febriel period
sensory loss rare
spinal variant
spinal nerve involvement
bulbar involvement
CN IX and X
polio tx
hospilatizaiton
skin precautions
ICU admin if resp sx
PT- long term
decorticate posturing
pathologic response to noxious stimuli
assault or injury to brain and or brainstem
abnormal flexion of the arms with extension of the lower extremities
sx of neuro injury not a dx
decerebrate posturing positioning
adduction and internal rotation at the shoulder
extension of elbows with flexedwrist/fingers
extension at the knees with plantar flexion of the ankle ad extension of toes
sx of neuro injury, NOT a dx
decorticate posturing
pointe dand turned intoes
arms bent toward center body
curled wrists nd balled hands against chest
decerebrate positioning
flexed wrists
curled fingers
straight tense arms prallel to body
decorticate and decererbrate posturing- what to check
CT vs MRI
tumor, trauma, hydrocephalus
CBC
CMP
hepatic encephalopathy
lead testing
infectious causes
malaria
encephalitis
CSF
frontal loeb funitons
motor cortex
sensory cortex
brocas area
personality
temporal lobe functions
-hearing
language- wernickes area
pariteal lobe functions
senses
taste
touh
smell
hearing
sight
occipital lobe functions
vision center
causes of cerebral injury
traumatic brain injury
stroke
ischemic
hemorrhagic
tumors
malignant vs benign
intracranialhemorrhage
aneurysms
ateriovenous malformations
encephalitis
neurodegenerativedz
alheimers
parkinsons
huntingtons
cerebral injury s/sx
memory loss
temporal lobe
impaired judegment
personality changes
sensory changes
visual
auditory
language changes
cerebral injury tx
surgery
meds
anticoags for CVA (not for hemorrhagic)
abx fro infections
PT
OT
speech therapy
cognitive therapy
cerebral injury pronosis
highly variable
permanent deficit vs partial vs full recovery
extent of injury
TIME to recognition and tx
access to care
cerebellar injury ddx
trauma
stroke
tumors
benign vs malignant
infections
hereditary ataxia
friedreichs ataxia
spinocerebellar ataxia
hemorrhgae
nauerysm
AVM
MS
etoh
vestribular disorders
cerebellar injury s/sx
ataxia
balance issurs
weakness
coordination issues
tremor
cerebellar dz tx
treat undelryign cond
sugery
meds
stop etoh
PT
balance
coordination
motor skills
cerebellar injury prognosis
typically, better tha cerebra
early recognition still very important
sccess to care
commitment to care