TBI & MS

TRAUMATIC BRAIN INJURY NEUROLOGICAL MANIFESTATIONS

- neurological dysfxn caused by an external force 1) Spasticity- velocity dependent resistance
- M>F, 15-25y/o - Modified Ashworth scale or Tardieu scale
Etiology: Falls (MC), MVA, Assaults, Sports 2) Cognitive Impairment- alteration of Attention,
Concentration, Executive fxn, Memory, Learning,
MECHANISM of INJURY Consciousness/Arousal level
1) Acceleration Injury- when a moving force hits the head Level of Consciousness:
2) Deceleration Injury- when a moving head meets a > Coma- (-)sleep/wake cycle, (+)ventilator
stationary object; ex: Head on collision > Vegetative Stage- (+)sleep/wake cycle, (-)self &
3) Coup Injury- injury of brain is at the site of impact environmental awareness, (-)ventilator
4) Counter Coup Injury- injury of head is opposite on site of > Persistent Vegetative Stage- poor prog (>30days or >1yr)
impact > Minimally Conscious State- (+)min. evidence of self &
environmental awareness, (+)visual tracking; MC
PATHOPHYSIOLOGY > Lethargic- mildly depressed; Can be fully aroused
PRIMARY BRAIN INJURY- occurs immediately p accident > Obtunded- more depressed; Can’t be fully aroused;
1) Diffuse Axonal Injury (DAI)- 2° high-velocity forces (acc-dec- Drowsy; Delayed reaction
angular); Shearing of subcortical axons c in myelin sheath > Stupor- unresponsiveness; Can be aroused briefly via
- Most distinguishing feature of TBI repetitive vigorous sensory stimulus such as pain
- Responsible for initial loss of consciousness & coma 3) Neurodevelopmental Impairment- mental inflexibility,
Sites: Corpus Callosum (MC), Parasagittal white matter, apathy, disinhibition/impulsivity, emotional lability, agitation/
Pons & Mb aggression, irritability
2) Concussion- 2° to shaking of brain; aka Mild TBI/Mild DAI; 4) Dysautonomia/Paroxysmal Sympa Hyperactivity/PAID
Alteration of consciousness syndrome- ↑HR, RR, MP, Hyperthermia, Diaphoresis,
Level of Consciousness: Coma, Vegetative Stage, Persistent Hypertonia, Decerebrate/Decorticate posture, Teeth grinding
Vegetative Stage, Minimally Conscious State, Lethargic, 5) Post Traumatic Seizure- Anti-convulsive drug (Phenytoin)
Obtunded, Stupor 6) Post Traumatic Amnesia- length of time from the injury
3) Contusion- aka Cortical bruises until the time which Pt remembers ongoing events
- 2° low-velocity forces such as falls & blows Dx tools: Galveston-Orientation & Amnesia Test (GOAT),
Sites: Inferior frontal lobe- behavioral changes Orientation Log Test (O-Log)
Anterior temporal lobe- memory loss 7) Others
a) HO- bone formation near the jt; MC site: Sh
SECONDARY BRAIN INJURY- occurs days or hours p accident b) Myositis Ossification
1) Hypoxic Ischemic Injury- brain tissue undergoes infarction c) Pneumonia
& death 2° to lack of 02/blood supply d) Pressure ulcer- bed turning q 2hrs
Cause: Systemic hypotension, Anoxia, Damage to the e) Fracture
vascular territories f) Contracture
2) ↑Intracranial Pressure- (N): 4-15/5-10mmHg g) Ms atrophy
TBI: >20mmHg h) DVT
- May damage CN 2 & May lead to brain herniation
- (+)Cushing sign/Hakims triad (bradycardia, bradypnea, SCALES
HTN)= Mx: Mannitol CLASSIFICATION OF SEVERITY
3) Herniations Mild Moderate Severe
a) Uncal- uncus of temporal lobe; MC type LOC 0-30 mins 30 mins-1day >1 day
- Cerebral peduncle (C/L hemiparesis), RAS (coma), PTA 0-1 days 1-7 days >7 days
Oculomotor n. (I/L gaze palsy), PCA (hemianopsia) GCS Score 13-15 9-12 3-8
b) Central/Transtentorial- diencephalon/thalamus
- Pons & Mb (decerebrate rigidity), RAS (coma)
GCS-40
c) Tonsilar- Cerebellar tonsils (neck pain), RAS (coma), MO
Eyes Motor Verbal
(alterations of HR, PR, RR), Indirect activation pathway
(flaccidity) 4- spontaneous 6- follows 5- oriented
4) Hydrocephalus- Normal Pressure Hydrocephalus- adult 3- to speech command 4- disoriented/
form- communicating type (sound) 5- localizes pain confused
- problem c reabsorption of CSF in arachnoid villi 2- to pain 4- withdraws to 3- inappropriate
Triad: “DIG” Dementia, Incontinence (urinary), Gait ataxia (pressure) pain (words)
Mx: Ventriculoperitoneal Shunt 1- no response 3- decorticate 2-
2- decerebrate incomprehensible
1- no response (sounds)
1- silent
GLASGOW LEIGE SCALE: 0- no reflex
1- oculo cardiac reflex
2- horizontal oculo cephalic
3- pupillary light reflex
4- vertical oculo cephalic
5- fronto-orbicular reflex
GLASGOW OUTCOME SCALE
8- good recovery upper; Can return to work completely
7- good recovery lower; Can return to work c some problems
6- moderate disability upper; Can return to work c modif.
5- moderate disability lower; Independent ADLs but not
returned to previous lifestyle
4- severe disability upper; 8hrs/day assistance
3- severe disability lower; 24hrs/day assistance
2- vegetative state
1- death
RANCHOS LOS AMIGOS - for cognitive functioning
I- No response- Pt is in deep sleep, Unresponsive to any
stimuli
II- Generalized response- responses are physiologic body
movt’s, limited & same, stereotypic, not related to stimulus
III- Localized response- now related to type of stimulus, May
follow simple commands inconsistent & delayed manner
IV- Confused Agitated- has bizarre behavior, Pt is in
heightened state of activity, No short/long-term memory
V- Confused Inappropriate- may follow simple commands
fairly consistent, Memory impaired, No learning is possible
VI- Confused Appropriate- may follow simple directions
consistently, Pt has goal directed behavior, Carry over of
relearned task
VII- Automatic Appropriate- has robot like behavior,
Judgement impaired, New learning at a ↓rate, Able to
initiate social & recreational act.
VIII- Purposeful Appropriate- environmental awareness,
Abstract reasoning, New learning s supervision
NEUROPLASTICITY
1) Use It or Lose It- failure to drive specific brain fxns can lead
to functional degradation
2) Use It & Improve It- training that drives a specific brain fxn
can lead to an enhancement of that fxn
3) Specificity- the nature of training experience dictates s the
nature of plasticity
4) Repetition Matters- induction of plasticity requires
sufficient repetition
5) Intensity Matters- induction of plasticity requires sufficient
training intensity
6) Time Matters- different forms of plasticity occur at
different times during training
7) Salience Matters- training experience must be sufficient
salient to induce plasticity
8) Age Matters- training induced plasticity occurs more
readily in younger brains
9) Transference- plasticity in response to 1 training
experience can enhance the acquisition of similar behavior
10) Interference- plasticity in response to 1 training
experience can interfere c the acquisition of other behavior
MULTIPLE SCLEROSIS
- aka Great Crippler of young adults
- Autoimmune dse of CNS
- Characterized by segmental demyelination, inflammation &
gliosis
Epidemiology: F>M (20-40y/o), Whites, High socioeconomic
status
Etiology: Idiopathic
Theories: 1) Autoimmune dse induced by a viral or other
infectious dse (Herpes viruses 1,2,6, Clamydial Pneumonia)
2) Genetics- MHC proteins encoded on Chr. 6
Pathophysiology: Demyelinated areas eventually become
filled c fibrous astrocytes & undergoes Gliosis/Astrocytosis
*Gliosis- refers to proliferation of neuroglial tissue c in the
CNS & results to glial scar (plaque, hallmark of MS)
*Astrocytosis- axon itself becomes interrupted & undergoes
retrograde regeneration
*MS- MRI, TBI: CT Scan
CLINICAL TYPES
Accdg. to Severity:
1) Benign MS- dse in which Pt remains fully fxnal in all
neurological systems 15yrs p onset
2) Malignant MS- aka Marburg’s dse; Rapid onset & almost
continual leading to significant disability or death c in a
relative short time period p onset
Major Subtypes:
1) Relapsing-Remitting- aka Exacerbating-Remitting; MC: 85%
- Characterized by discrete attacks of neurological deficits
(relapses) c either full or partial recovery (remission) in
subsequent wks to mos.
Onset: Sensory (Paresthesia, Optic Neuritis)
- RR c complete & incomplete remission (MC)
2) Secondary Progressive- 20% of Relapsing-Remitting
becomes progressive; 2nd MC
- Characterized by an initial RRMS course c progression to
steady & irreversible decline c or s continued acute attacks
3) Primary Progressive- 10%; Progressive dse c little to no
attacks; Later onset; M>F (40y/o); Motor onset;
Polysymptomatic onset; Fewer MRI lesions
- Characterized by a nearly continues worsening of the dse
from onset s distinct attack
4) Progressive-Relapsing- 5%, LC; Progressive disease c series
of attacks later in the course
SITES OF PREDILECTION
> Periventricular white matter
> Post. white column of SC
> Optic nerve
> Brainstem
> Cortex, Corticospinal Tract, Cerebellum
CHARCOT’S TRIAD/CARDINAL SIGNS: “SIN” Scanning speech,
Intention tremor, Nystagmus
CLINICAL MANIFESTATIONS
1) SENSORY SYSTEM- Paresthesia (MC presenting sx), Pain
(electric-like)
Face- CN5= Tic Douloureux, Paroxysmal Pain Dysfunction
 Limb- Dysesthetic limb= Paroxysmal limb pain- MC type of 3.5 Moderate disability in 2 functional system
pain (LE>UE) 4 Full amb. s rest & assist in 500m
Trunk- “MS Hug”- painful band sensation around trunk 4.5 Full amb. s rest & assist in 300m
Headache- MC pain complaint 5 Full amb. s rest & assist in 200m
Hyperpathia- sensitivity to light stimulus 5.5 Full amb. s rest & assist in 100m
2) VISUAL SYSTEM 6 Intermittent unilat. assist in 100m c/s resting
> Optic Neuritis- ice pick like sensation behind eye c 6.5 Constant bilat. assist in 20m s resting
blurring/graying of vision that leads to blindness 7 Unable to walk beyond 5m
> Nystagmus 7.5 Can’t take few more steps, Needs W/C
> Diplopia/Ophthalmoplegia 8 Bed bound, Can be out of bed much of the day
> Scotoma- dark spots in the visual field
8.5 Bed bound much of the day
3) BRAINSTEM
9 Bed ridden, Can eat, talk & swallow
> CN 2,5,7,8
9.5 Bed ridden, Can’t eat, talk & swallow
> Dysarthria (Scanning speech)
10 Death
> Dysphagia & Dysphonia (CN 9,10)
4) PYRAMIDAL SYSTEM
> UMNL- LE>UE (spasticity, paresis, hyperreflexia,
hypertonia, (+)Babinski, gait ataxia)
> Fatigue- MC sx; Most troubling & disabling; Worst in hot
> Uhthoff’s phenomenon- anything that ↑body temp leads
to Pseudoexacerbation of sx
- once body temp is (N), s/sx may improve or disappear
Criteria: <24hrs, Reversible
5) COGNITIVE- Dementia, Attention tremor, Memory loss
6) CEREBELLAR SYSTEM
> Intention Tremor
> Uncoordinated movements- dysmetria, dyssynergia,
dysdiadochokinesia, gait ataxia (drunkenness)
7) BOWEL & BLADDER
> MC bowel- Constipation
> MC bladder- Detrusor Hyperreflexia, Spastic, Dyssynergic
8) SEXUAL
> Female- loss of sensation & libido, difficulty reaching
orgasm, vaginal dryness
> Male- loss of sensation & libido, difficulty ejaculation,
impotence

PROGNOSIS
GOOD- Female (<40y/o), Sensory onset, 1 sx at onset, RRMS
POOR- Male (>40y/o), Motor onset, Polysymptomatic onset,
PPMS & PRMS

PHARMA Mx
1) Immunosuppressive drugs- for acute flare-ups (shortens
duration of period/attack)
- ex: Prednisone, Dexamethasone
2) Interferon Beta drugs- slow down dse. progression
- ex: Betaferon, Extavia, Plegridy, Avonex, Rebif
3) Anti-spasticity drugs- Dantrolene, Baclofen
4) Anti-cholinergic drugs- for bladder dysfxn

KURTZKE EXPANDED DISABILITY SCALE

0 Normal
1 No disability; Minimal sx in 1 functional system
1.5 No disability; Minimal sx in 2 functional system
2 Minimal disability in 1 functional system
2.5 Minimal disability in 2 functional system
3 Moderate disability in 1 functional system