TRAUMATIC BRAIN INJURY - brain comes into contact with

● An alteration in brain injury function, or other bony protuberances on inside

evidence of brain pathology caused by an surface of the skull
external force - damage from the penetrating
○ Brain damage external forces that cause object
brain tissue to make direct contact with - Contusions, lacerations, mass
an object rapid acceleration or effect from hemorrhage and
deceleration forces, or blast waves from edema (hematoma).
an explosion 2. Diffuse axonal injury (DAI)
● Most challenging patient ● caused by rapid
- Little progress or maintenance problem acceleration/deceleration of the
● Multiple body systems affected by a brain injury brain
● Strong likelihood of secondary impairments ● acceleration/deceleration forces
● TBI requires a strong interdisciplinary team cause disruption of
neurofilaments within the axon
TBI EPIDEMIOLOGY leading to Wallerian-type axonal
● Leading cause of injury related death and degeneration
disability in the US ● DAI most often occurs in
● Approximately 1.7 million people admitted to discrete areas:
emergency departments with TBI yearly - parasagittal white
● Children, adolescents less than 25 years old matter of the cerebral
● Older adults are most at risk for experiencing cortex › corpus
TBI callosum
○ Most common in young children 0-4 y/o - pontine-mesencephalic
○ Hospitalization and death as a result of junction adjacent
TBI is most common in older adults 65 to the superior
y/o and over cerebellar peduncles
● Approximately 5.3 million people living in the US ● Mechanism of DAI is
are disabled as a result of TBI microscopic
● 4 out of 10 are not working 1 yr after injury 3. Blast injury
● Shock wave is produced when
TBI ETIOLOGY an explosive device detonates
1. Falls which can cause brain damage
- leading cause of TBI - 32% ● Primary blast injury
- Common in geriatric patient - results from the direct
2. Motor vehicle accidents (MVA) effect of blast
3. Assaults overpressure on organs
● Secondary injury
PATHOPHYSIOLOGY - results from shrapnel
and other objects being
● Primary injury hurled at the individual
- due to direct trauma to the parenchyma ● Tertiary injury
● Primary TBI - occurs when the victim
1. Focal injury is flung backward and
- bony skull or external object strikes an object
such as a bullet or sharp - Wall tas tumama ka
instrument creating a 4. Concussion
penetrating injury ● Loss of consciousness, either
- often result in contusions, temporary or permanent,
lacerations and intracerebral resulting from injury or blow to
hematomas head
- generally focal in nature ● Impaired functioning of the
brainstem reticular activating
system (RAS)
 ● may see changes in HR, RR, ● forwards and backwards over
BP
a. Mild concussion syndrome the ridged cranial fossa inferior
- Momentary loss of frontal lobes and temporal poles
consciousness or
confusion after TBI are the commonest affected
- may see retrograde areas. contusion may lead to
amnesia
- (loss of memory that intracerebral hematoma → mass
goes back in time effect
before the injury
● focal neurological deficit
occurred)
● Hemiparesis
● speech disorder
● memory abnormalities
● visual dysfunction
● Has area of necrosis infarction
and hemorrhage
● Often from coup - contrecoup
injury
● Seizures are common after
contusion
● Coup & countre-coup injuries
b. Classical concussion - injury at point of impact
- moderate in severity and opposite point of
with loss of impact
consciousness ● Common sites:
- that is transient and - undersurface of frontal
mostly reversible in 24 lobe
hours; - tip of temporal lobe
- may see both
retrograde and post-
traumatic amnesia
(PTA: loss of memory
for events after the
traumatic event)
- temporary lethargy
- Irritability
- Cognitive dysfunction
c. Severe concussion
- Loss of Consciousness
for longer than 24 hour
- Associated with diffuse
axonal injury and coma
5. Cerebral contusion
● bruising of the brain - Contused cranial nerve is CN 1
● breakdown of small vessels
and extravasation of blood into Cushing’s Triad
the brain - Bradycardia
● coup or contrecoup injury - Hypertension
- abnormal respiration
● Sudden
- increased ICP: bradycardia, bradypnea,
acceleration/deceleration → hypertension
- symptoms of ICP is opposite of shock
brain slides
Impairments Commonly Associated with TBI
1. Neuromuscular Impairments
• paresis Upper extremity (UE) and lower
extremity (LE)
• impaired coordination
• Impaired postural control
• abnormal tone
• abnormal gait
• Abnormal involuntary movements such
as tremor and choreifor
• dystonic movements are less common
• impaired somatosensory function
2. Cognitive Impairments
Cognition
- mental process of knowing and applying
information includes many complex
neural processes, including: arousal,
attention concentration, memory,
learning, executive functions
- planning, cognitive flexibility, initiation
and self-generation
- response inhibition
- serial ordering and sequencing
A. Altered levels of Consciousness
• Coma, vegetative state & minimally
conscious state
• Coma
- Arousal system is not functioning
- No sleep/wake cycles
- Ventilator dependent
- No auditory or visual function›
- No cognitive or communicative function
- Abnormal motor and postural reflexes
may be present
- May become brain dead
- May enter a vegetative or minimally
conscious state, or go onto full recovery.
B. Vegetative state
- dissociation between wakefulness and
awareness
- brainstem is able to manage basic
cardiac & respiratory functions
- sleep/wake cycles are present
- may startle to visual or auditory stimuli
cognitive and communication function is
absent
- Reflexive smiling/crying may be present
Neuromuscular
- Presis
- Abnormal tone
C. Minimally conscious state
- Cognitively mediated behaviors occur
inconsistently
- Sleep/wake cycles are present
- Withdrawing or posturing to noxious stimuli
and can localize source of stimuli
- Stupor: strong/ noxious stimuli
- Obtunded state: vigorous, repeated sensory
stimulation
- Sleeps often
- when aroused exhibits decreased alertness
delayed reactions
3. Neurobehavioral Impairments
• Profound behavioral changes
• behavioral sequelae include:
- Low frustration tolerance
- Agitation
- Disinhibition
- Apathy
- Emotional Lability
- Mental inflexibility: cannot think
properly
- Aggression
- Impulsivity
- Irritability
4. Communication
• Language and communication deficits include:
- disorganized and tangential oral or
written communication
- imprecise language
- word retrieval difficulties
- disinhibited and socially inappropriate
language
5. Dysautonomia
• Increased sympathetic activity results in:
- ''Paroxysmal sympathetic hyperactivity
- Increased heart rate respiratory rate,
and blood pressure, diaphoresis and
hyperthermia
- Decerebrate and decorticate posturing,
hypertonia and teeth grinding
6. Post-traumatic Seizures
• Phenytoin (an anticonvulsant):
- decreases the risk of early post-traumatic
seizures.
- Develops in severe TBI
Cognitive
- Arousal level
- Attention
 - Motor function - Concentration Oriented 5
- Postural control - Memory Confused Conversation 4
- Learning Inappropriate words 3
- Executive Function Incomprehensible sounds 2
Neurobehavioral Communication No response 1
- Agitation/Aggression - Language and
- Disinhibition communication - 15 is normal
- Apathy disorders
- Emotional Lability - Swallowing
- Mental inflexibility - Dysphagia PEDIATRIC GLASGOW COMA SCALE
- Impulsivity Activity Score
- Irritability Eye Opening
Spontaneous 4
SECONDARY IMPAIRMENTS To speech 3
• Deep vein thrombosis To pain 2
No response 1
- examination tool: Well’s criteria
Best Motor Response
• Heterotopic Ossification (SCI due to aggressive Normal spontaneous 6
stretching) movement
• Pressure ulcer Withdraws to touch 5
• Pneumonia Withdraws to pain 4
• Chronic pain Abnormal Flexion 3
Abnormal extension 2
• Contractures
No response 1
• Decreased endurance Verbal Response
• Muscle atrophy Coos, Babbles 5
• Fracture d/t injury Irritable cries 4
- orthostatic hypotension Cries to pain 3
- gradually increasing the bed Moans to pain 2
• Peripheral nerve damage No response 1

Diagnosis and Prognosis HOW OFTEN SHOULD OBSERVATIONS BE

1. Glasgow Coma Scale (GCS) RECORDED?
- most widely used clinical scale that • Frequency of observation
measures level of consciousness - observations should be performed and recorded
- helps define and classify the severity of on a half hourly basis until GCS equal to 15 has
injury been achieved. If GCS = 15 observ3e: half hourly
for 2 hrs then 1 hourly for 4 hrs then 2 hourly
2. Scores Mild Head Injury
thereafter: should the patient with GCS equal to 15
- Scores of 13 to 15
deteriorate at any time after the initial 2-hr period
3. Moderate Head Injury
observations should revert to half-hourly
- Scores between 9& 12
• Urgent reappraisal by the supervising doctor
4. Severe Head Injury
- a sustained (that is for at least 30 mins) drop of
- Scores of 8 or less
- Lowest score is 3
one point in GCS level (greater weight should be
given to a drop of one point in the motor score of
Activity Score the GCS)
Eye Opening - any drop of 3 or more points in the eye-opening
Spontaneous 4
or verbal response scores of the GCS or 2 or more
To speech 3
points in the motor response
To pain 2
No response 1
Best Motor Response
Follows motor commands 6
Localizes 5
Glasgow Outcome Scale
Withdraws 4
Abnormal Flexion 3 5 Good Recovery Light damage w/ minor
Extensor response 2 neurological and
No response 1 psychological deficits
Verbal Response 4 Moderate No need for assistance in
Disability everyday life, employment is
 possible but may require - Galveston Orientation and Amnesia Test
special equipment (GOAT),
3 Severe Severe Injury w/ permanent - PTA less than 27 days are likely to be
Disability need for help w/ daily living employed
2 Persistent Severe damage w/ prolonged
- PTA less than 34 days
vegetative state of unresponsiveness
state and a lack of higher mental are likely to have a good overall recovery
functions - PTA less than 53 days are likely to be living
1 Death without assistance

GLASGOW OUTCOME SCALE- EXTENDED CHARACTERISTICS OF MILD, MODERATE AND

SEVERE TBI
Mild Moderate TBI Severe
TBI TBI
LOC 0-30min >30min and >24
24<hr
AOC Brief >24 >24
>24
PTA 0-1 day >1 and 7< days >7 days
GCS 13-15 9-12 <9
Neuroimaging: Normal Normal or Normal or
abnormal Abnormal
DIAGNOSTIC TESTS
● CT Scan
● MRI
GALVESTON ORIENTATION AND AMNESIA TEST
● Transcranial Doppler studies
(GOAT)
- Looking for vasospasm EEG
• Score: for post-traumatic amnesia (Adults)
● No lumbar puncture if there is IICP because
• Normal: 76-100 points sudden release of pressure can cause brain to
• - <75: amnesic herniate
• - iNormal: > 75 for 2 consecutive days ● ABG’s –keep O2 at 100% and PCO2 as related
to ICP (25-35)
● Increase ICP = no lumbar puncture

INVESTIGATIONS
• Skull radiograph

• CXR and X-ray of cervical spines

• CT-Scan -first line investigation

Medical Management
Prognosis
● Factors associated with poor outcomes are: • Medical treatment following brain injury starts at
- Age the scene of the accident
- Race
● Early resuscitation with the goal of stabilizing the
- Lower education level
cardiovascular and respiratory systems is
● Predictive of poor outcome
important Maintain sufficient blood flow and
- Petechial Hemorrhages
oxygen to the brain
- Subarachnoid bleed
● Primary goals are:
- Obliteration of 3rdventricle or basal cisterns
○ to minimize secondary brain injury by
- Subdural hematoma
optimizing cerebral blood flow and
● Higher Functional Independence Measure (FIM)
oxygenation
scores at discharge
○ stabilize vital signs
● Duration of post-traumatic amnesia
○ perform a complete examination
- length of time between the injury and the time
○ identify and treat any non-neurological
when memory returns
injuries
 ○ continuously monitor the patient
Rancho Los Amigos Levels of Cognitive Functioning
(LOCF)
I. No Response
● Patient appears to be in a deep sleep
completely unresponsive to any stimuli
II. Generalized Response
● Patient reacts inconsistently and non-
purposefully to stimuli in a nonspecific manner
● Responses are limited and often the same
regardless of stimulus presented
● Responses may be physiological changes,
gross body movements and/or vocalization.
III. Localized Response
● Patient reacts specifically but inconsistently to
stimuli
● Responses are directly related to the type of
stimulus presented.
● May follow simple commands such as closing
eyes or squeezing hands in an inconsistent,
delayed manner.
IV. Confused-Agitated
● Patient is in a heightened state of activity
● Behavior is bizarre and non-purposeful
relative to immediate environment
● Does not discriminate among persons or objects
● Unable to cooperate directly with treatment
efforts
● Verbalizations
● Frequently are incoherent and/or inappropriate
to the environment Confabulation may be
present
● Gross attention to environment is very brief
Selective attention is often nonexistent
● Patient lacks short-and long-term recall
● Special considerations:
○ Encourage repetition for consistency
○ Increase safety precautions
○ Calm behavior and environment
○ Expect no carry over of learning
V. Confused-Inappropriate
● Patient is able to respond to simple commands
fairly consistently. Responses are non-
purposeful, random, or fragmented.
● Demonstrates gross attention to the
environment but is highly distractible
● Lacks ability to focus attention on a specific
task
● May be able to converse on a social automatic
level for short periods of time
● Verbalization is often inappropriate and
confabulatory.
● Memory is severely impaired
● Often shows inappropriate use of objects
● May perform previously learned tasks with
structure but is unable to learn new information
VI. Confused-Appropriate
● Shows goal-directed behavior but is dependent
on external input or direction.
● Follows simple directions consistently and
shows carryover for relearned tasks such as
self-care.
● Responses may be incorrect due to memory
problems, but they are appropriate to the
situation
● Past memories show more depth and detail than
recent memory.
VII. Automatic-Appropriate
● Patient appears appropriate and oriented within
the hospital and home settings
● Goes through daily routine automatically, but
frequently robot-like.
● Shows minimal to no confusion
● Has shallow recall of activities.
● Shows carryover for new learning but at a
decreased rate. (new exercise)
● With structure is able to initiate social or
recreational activities; judgment remains
impaired.
VIII. Purposeful-Appropriate
● Patient is able to recall and integrate past and
recent events and is aware of and responsive to
the environment.
● Shows carryover for new learning
● Needs no supervision once activities are learned
● May continue to show a decreased ability
relative to premorbid abilities, abstract
reasoning, tolerance for stress, and judgment in
emergencies or unusual circumstances.
Coma Recovery Scale Revised (CSR-R)
- The Coma Recovery Scale–Revised (CRS-R) is
recommended to assess patients with
disordered consciousness.104 The CRS-R is a
valid and reliable 23-item measure with six
subscales: auditory, visual, motor, oromotor,
communication, and arousal.105 Scores range
from 0 to 23. Data are useful in distinguishing
between different states of consciousness
 (vegetative state, minimally conscious state, and
emerging), determining the prognosis, and
informing treatment planning.
DISORDERS OF CONSCIOUSNESS SCALE (DOCS)
- The Disorders of Consciousness Scale (DOCS)
is a valid and reliable scale also designed to
measure arousal and neurobehavioral recovery
in patients with disorders of consciousness. It
consists of 23 items, which assess social
knowledge, taste/swallowing, olfactory function,
proprioception, tactile sensation, auditory
function, and visual function. Scoring is based
on patient response and includes no response,
generalized response, or localized response.
- The DOCS can be used to differentiate states of
consciousness (i.e., vegetative state and
minimally conscious state) and assist in
determining prognosis for recovery.
• General goals and outcomes anticipated for
patients with severe to moderate traumatic brian
injury in the acute stage
o Physical function and level of alertness
are increased
o The risk of secondary impairments is
reduced
o Motor control is improved
o The effects of tone are managed
o Postural control is improved
o Tolerance of activities and positions is
increased
o Joint integrity and mobility are improved
or remain functional
o Family and caregivers are educated on
patient’s diagnosis, physical therapy
interventions, goals and outcomes
o Care is coordinated among all team
members

SEQUELAE OF TBI
INTERVENTIONS
• Neuromuscular
• Preventing secondary impairments
o Tone
• Susceptible to indirect impairments such as:
o Irregularities
o Contractures
o Sensory
o Decubitus ulcers
o Motor control
o Pneumonia
o Balance
o DVT
• Behavioral
1. ROM should be monitored
o Impulsiveness
• Serial casting may be used to maintain or
o Apathy
improve ROM
o Aggressive
• Often used for plantar flexor or biceps
o Lack of concern
contractures due to increase tone or
o Egocentricity
shortening
o Sexual appropriateness
• After 2-5 days the cast is removed
o Orientation
• Muscle is stretched again and another
o Attention
cast is applied
• Cognitive
• Monitor the patient after the cast is
o Amnesia
applied
o Retrograde
2. Proper positioning
o Anterograde
• Both in bed and in a wheelchair is
o Post traumatic
essential
o Procedural memory
o Declarative memory • Splints may be used to assist in
o Executive functioning positioning
• Swallowing • Turning will help prevent skin
o Communication breakdown and pneumonia
o Visual deficits • Air mattresses can be used to prevent
pressure sores
PLAN OF CARE (INTERVENTIONS DURING THE • Proper wheelchair or a tilt-in- space
ACUTE STAGE) wheelchair is typically required
- LOCF 3 • Proper pelvic positioning and head
positioning are key elements
3. Early mobility
 • Upright sitting is extremely important o A phenomenon whereby items that are
• As soon as medically stable self-generated are better learned and
• Patient should be transferred to a sitting remembered compare to information that
position is provided
• Out of bed to a wheelchair o As the cognitive and behavioral barriers
• All precautions should be observed to treatment become less intrusive,
• Head should be properly supported sessions can be progressively more
• Use of a tilt table is also advantageous challenging both mentally and physically
4. Sensory stimulation • Random practice schedule
• Increase the level of arousal o May be more beneficial to learning but
• Elicit movement in individuals in a coma schedule can be
or persistent vegetative state o Employed only after the patient has
demonstrated some
• Reticular activating system may be
o Initial learning of the task’s dynamics
stimulated by providing stimulation in a
controlled and multisensory manner • Feedback is also very important
o Explicit or augmented feedback
• Causing a general increase in arousal
o May be more beneficial in the early stages
• Multisensory stimulation involves the
of motor
presentation of sensory stimulation in a
o Learning as opposed to intrinsic feedback
highly structured and consistent manner
- verbal cues, motivation
PLAN OF CARE (INTERVENTIONS DURING THE
ACTIVE STAGE)
• PT should determine the patient’s cognitive
• Restorative Vs Compensatory based intervention
abilities, because these will affect the ability to
o Two basic strategies:
relearn motor skills
Compensatory approach
• Key initial question that warrants consideration - seeks to improve functional
include the following: skills by compensating for the
o Is the patient able to follow commands: lost ability
one-step, two- step or multistep - ex: teaching one hand resting
commands? technique, teaching to
o Is the patient oriented to person, place, compensate
and/ or time? Restorative approach
o Does the patient recognize family - seeks to restore the “normal”
members? use of the affected extremity
o Does the patient demonstrate any insight
into what has happened?
COMPENSATION VS RESTORATION: GUIDING
• Motor (Re)Learning strategies
QUESTION TO CONSIDER
o Treatment sessions should be
thoughtfully planned
o Practice should be distributed, with
frequent rest periods
o Patients may experience mental as well as
physical fatigue
o Signs of mental fatigue may include:
Increased irritability
Decreased attention and
concentration
Deterioration in performance of
physical skills
o Provide sufficient rest period to minimize
both physical and mental fatigue
• Self-generation concepts
 o The training experience must be
sufficiently salient to induce plasticity –
salient matters
o Plasticity in response to one training
experience can enhance the acquisition of
similar behaviors – transference
o Plasticity in response to one experience
can interfere with the acquisition of other
behaviors – interference
o Training- induced plasticity occurs more
readily in younger brains – age matters
• Locomotor training with body weight support
o Locomotor training with BWS is
commonly combined with treadmill
ambulation
o PTs assist the patient by providing
trunk/pelvic stabilization, assistance with
weight shifting and advancing the LE
• Hybrid assistive limb therapy
o Cyberdyne
• Gait therapy using C- Mill by Motek

• Restorative interventions and Neural plasticity

o Current research has demonstrated task
specific interventions with large amounts
of practice can induce beneficial
neuroplastic changes in the CNS and
restore function
• 10 principles of experience dependent
neuroplasticity
• Constraint- Induced therapy
o Failure to drive specific brain functions
o Involves promoting the use of the more
can lead to functional degradation – Use
affected UE for up to90% of waking hours
it or lose it
reducing the use of the least affected UE
o The nature of the training experience
• Electrical stimulation
dictates the nature of the plasticity –
o Application of FES
specificity
o FES foot-drop stimulators
o Induction of plasticity requires sufficient
o Rely on peroneal nerve stimulation to
repetition – repetition matters
increase active dorsiflexion during the
o Training that drives a specific brain
swing phase
function can lead to an enhancement of
• Dual-task performance
that function – use It and improve it
o Progressively more challenging cognitive
o Different forms of plasticity occur at
tasks
different times during training – time
o Example: walking on a treadmill while
matters
reading
o Induction of plasticity requires sufficient
• Patient/f family/ caregiver education
training intensity – intensity matters
 o Educate and train the patient family and - Young adults
caregiver important to emphasize safety - (+) VOR (dolls eye sign)
awareness education with the patient and - PTA < 4 wks
caregivers - Coma < 1 wk
• CCS <8
- late adults
- (-) VORD
- PTA > 12 wks

- coma > 2 wks

LOCF I-III
• Management based on decreased response level
o Maintain ROM, prevent contracture
development
o Maintain skin integrity
o Maintain respiratory status, prevent
complications
o Provide appropriate stimulation for
arousal and to elicit movement and
function; structure environment to
enhance alertness and function
o Promote early return to functional
mobility skill

LOCF IV-VI
• Management based on mid-level recovery
o Provide structure, prevent
overstimulation for confused, agitated
patient
o Provide consistency
o Engage patient in task-specific training
o Provide verbal or physical assistance
o Control rate of instruction
o Emphasize safety, behavioral
management techniques
o Model a calm, focused behavior

LOCF VII-VIII
• Management based on high-level of recovery
o Allow for increasing independence
o Assist patient in behavioral, cognitive,
Emotional reintegration
o Enhance motor learning and promote
independence in functional tasks
o Improve postural control, symmetry and
balance
o Encourage active lifestyle, improve
cardiovascular endurance

PREDICTOR OF OUTCOMES
• CCS >8
SEIZURE (TBI)
• Are disorders characterized by excessive or CAUSES
over synchronized discharges of cerebral 1. Benign febrile convulsions of childhood
neurons 2. Idiopathic epilepsy
3. Head trauma
SYNCOPE 4. Stroke
• Loss of consciousness due to a reduced supply 5. Mass lesion
of blood to the cerebral hemispheres or 6. Meningitis or encephalitis
brainstem
• Caused by pan cerebral hyperperfusion SYSTEMIC DISORDERS
1. Hypoglycemia
PHENOMENA AT ONSET OF SPELL • Decrease for 30-40mg
1. An ambiguous description of a sudden of onset 2. Hyponatremia
of unconsciousness without prodromal features • Lower than 120 serum sodium
is highly suggestive of seizures 3. Hyperosmolar state
• Primary ora • High potassium, sodium,
2. Focal sensory or motor phenomena (E.g., • Hypercalemia
involuntary jerking of one hand, hemifacial paresthesias, 4. Hypocalcemia
forced head turning) suggests a seizure originating in the 5. Uremia
contralateral frontoparietal cortex 6. Hepatic encephalopathy
3. A sensation of fear, olfactory or gustatory 7. Porphyria
hallucinations or visceral or deja vu sensations are • Disorder of hemoglobin
commonly associated with seizures originating in the • Can produce neuropathy and seizures
temporal lobe 8. Drug overdose
4. Progressive light-headedness, dimming of vision 9. Drug withdrawal
and faintness which indicate diffuse central nervous 10. Global cerebral ischemia
system dysfunction are associated with decreased • Caused by hypovolemia, cardiac arrest,
cerebral blood flow from any cause (Simple faints, hypotension
cardiac arrhythmias, orthostatic hypotension) 11. Hypertensive encephalopathy
12. Eclampsia
EVENTS DURING THE SPELL 13. Hyperthermia
• 3-5 mins (ictal stage)
• More than 5 mins = general cerebral CLASSIFICATION AND CLINICAL FINDINGS
hypoperfusion • Generalized seizures
1. Generalized tonic-clonic o Tonic- clonic (grand mal)
• Nanginginig • Arch back
2. Cerebral hypoperfusion usually produces flaccid o Absence (petit mal)
unresponsiveness • Tulala na but he/ she is awake
• Might lead to permanent damage o Other types (tonic, clonic, myoclonic)
• Want to happen as short as possible • Partial seizures
• Seizures one part of the body
o Simple partial
PHENOMENA FOLLOWING THE SPELL (POST- o Complex partial (temporal lobe,
ICTAL STAGE) psychomotor)
1. A period of confusion, disorientation or agitation • Feeling of paranoia, scared then
(postictal state) it may lead to absence
2. Prolonged alteration of consciousness
(prolonged postictal state) GENERALIZED SEIZURE
• Somnolent • Generalized tonic-clonic seizures
• The longer the seizure the longer the o Tonic phase
ictal state o Clonic phase
• Works when you smell something to o Recovery
patient • 10-30 mins
• 3 mins unconsciousness after seizure, • Absence (petit mal) seizures
call ambulance because its emergency • Unconsciousness 5-30 secs for as long
3. Recovery from a simple faint is characterized by as 30 mins without loss of posture
a prompt return to consciousness with full lucidity • Subtle head turning

CHRONIC DISORDERS OTHER TYPES OF GENERALIZED SEIZURES

1. Multiple sclerosis 1. Tonic seizures
2. TBI/ Stroke 2. Clonic seizures
 3. Myoclonic seizures 8. Spondylosis
• Violent 9. Osteogenesis imperfecta: bone fragility
4. Atonic seizures
• Conscious but no tone
• Aka drop attack PATHOPHYSIOLOGY
• Like the patient is dead - produce in association with the vertebral column

PARTIAL SEIZURES - most common mechanism would be fracture of one or

1. Simple partial seizures more of the bony elements that could happen in
• Distortion of memory osteoporosis, spinal arthritis and…
• Patient can be conscious or - dislocation of one or more joint: ankylosing spondylosis
unconscious
2. Complex partial seizures - tear of ligament = lesser support
• Called before psychomotor seizure - disruption and/or herniation of IV disk
• Whole right body seizes but patient is
- fracture, dislocation
conscious
• Arises from temporal and medial
temporal lobe

PHARMACOTHERAPEUTIC CLASSIFICATION OF SPINAL INJURY

• Phenytoin (dilantin) 1. Flexion
• Carbamazepine (tegretol) 2. Flexion- rotation
• Phenobarbital 3. Extension
• Valproic acid 4. Vertical compression
• Clonazepam
• Gabapentin - functional categories: tetraplegia and paraplegia
- tetraplegia/ quadriplegia: all 4 limbs plus the trunk
(Respiratory muscle) are paralyzed
- paraplegia: both lower extremity and part of the trunk is
SPINAL CORD INJURY paralyzed, spared upper extremities

SCI SYNDROMES
EPIDEMIOLOGY 1. Central cord syndrome
• Affected part
- cervical region
ETIOLOGY
• Mechanism of injury:
- male is more prominent because they are young active - hyperextension injuries to cervical
patient region
- mostly d/t motor vehicular accident/ violence (develop • Clinical manifestation:
countries) - weakness in upper extremity, varying
- least is due to sports accident or elderly degrees of sensory impairment
- UE is most affected than LE
- gunshot wounds
- high chance of ambulation
- possibly preserved/ spared: bowel and
SPINAL DISEASES -? TRAUMATIC SCI bladder function and Sexual function
- penetrating injury that causes spinal cord to be injured 2. Anterior cord syndrome
• Affected part
1. Spina bifida
- corticospinal tract and spinothalamic
- pediatric version of traumatic SCI
tract
2. Spinal stenosis
• Mechanism of injury
3. Transverse myelitis
- flexion injuries of cervical region and
4. Vascular dysfunction
damaged in anterior portion of the cord
5. Fruitridge ataxia
• Clinical manifestation
6. Tethered board
- paralysis mid loss of pain
- congenital condition
- spared proprioception, light touch and
7. Spinal arthritis
vibratory sense
 - different blood supply (posterior spinal
artery)
- has longer length of stay than the other
syndromes in the hospital
3. Transient paralysis and Spinal shock
• Affected part
• Mechanism of injury
• Clinical manifestation
4. Brown Sequard syndrome
• Affected part
- lateral spinothalamic tract
• Mechanism of injury
- hemi section of spinal cord
- caused by penetration wounds via
gunshot or stab wounds
• Clinical manifestation
- ipsilateral side: paralysis, sensory loss
and vibratory sense
- contralateral side: no sense of pain and
temperature
- lateral spinothalamic tract: ascends 2-4
segments on the same side before they
cross, whatever information they are
carrying they will cross it to other side
- “transient paralysis”: with complete recovery, young
patient’s with athletic injury, independent from spinal
shock, upon re-assessment of outcome measure it turns
out that they recover fully, they could have SCI but not
that intense, gives ASIA grade E
- loss of reflex activity: DTR, bulbocavernosus reflex and
cremasteric reflex
- bulbocavernosus reflex: pinky finger insert it to the butt
area to patient then glans penis hatakin and pagka babae
clitoris hahatakin then dapat may anal reflex, with gloves
and petroleum jelly which is done in side lying position
- could last for days, several hours or weeks
- depends on the attending physician how frequent the
patient should assess
- early = frequent assess
- 3 months = mas matagal na yung assessment
COMPLETE VS INCOMPLETE INJURY
- Complete: both sensory and motor loss below the lesion
up to S4 and S5, no presence of deep anal pressure and
voluntary anal contraction
- Incomplete: either one of them is intact or both is intact

CLINICAL MANIFESTATIONS
- Depending on SCI and ASIA OM

ASIA IMPAIRMENT SCALE

• Neurological level
- most caudal or inferior level of spinal cord with
both normal motor and sensory
• Motor level
- most caudal segment of Spinal cord with
intact/normal motor function bilaterally
- determined by testing the strength of MMT of
both sides of the body
• Sensory level
- lowest spinal cord level with normal testable pin
prick and touch sensation
- L5 Left: normal is the Right, Left S1 is abnormal
• Zones of partial preservation
- only used in complete SCI
SPINAL SHOCK - no function of S4 and S5
- Loss of all spinal cord function caudal to the level of the
injury
1. Flaccid paralysis
2. Anesthesia
3. Absent bowel and bladder control
4. Loss of reflex activity
5. Priapism (in males)
- lantang gulay ang tutoy
6. Bradycardia and hypotension
 2. Middle
- PLL
- Posterior annulus
- posterior wall VB
3. Posterior
- SSL/ISL
- posterior arch
- facet capsule
- ligamentum flavum

THE THORACOLUMBAR SPINAL CORD INJURY

CLASSIFICATION SEVERITY SCORE

• A=complete
- no motor or sensory function is preserved in the
sacral segments S4 to S5
• B=incomplete
- sensory but not motor function is preserved
below the neurological level and includes the sacral
segments S4 to S5
• C=incomplete
- motor function is preserved below the
neurological level, and more than half of key - proposed as an alternative
muscles below the neurological level have a muscle
grade less than 3 - CT Scan or MRI or X-ray to score or use this
• D=incomplete - <4 = non operative injury
- motor function is preserved below the - >4 = needs to operate
neurological level, and at least half of key muscles
- 4 = surgeon’s decision if they need to operate or not
below the neurological level have a muscle grade of
3 or more - 2005 released
• E = normal MEDICAL COMPLICATIONS
- motor and sensory function is normal • Cardiovascular complications
DENIS THREE COLUMN MODEL o Neurogenic shock
o Hemodynamic shock
- for surgical indications
o Bradycardia
o Cardiac arrythmia
• PT CONCERN
- maintain a mean arterial pressure of at least 85-
90 mmHg always
- mean arterial pressure = diastolic pressure + 1/3
systolic pressure – diastolic pressure
- ex: pt has currently 90/70mmHg
- ans: 77mmHg
• Respiratory complications
o Pneumonia & Pulmonary edema
- month na si patient
1. Anterior - highest with cervical lesion to be
- ALL followed by thoracic lesion
- anterior annulus - higher lesion = lesser physical activities =
- anterior wall VB high complications
 o Respiratory failure
- no ventilatory
- signs: increase RR, decrease force vital
capacity, rising carbon dioxide pressure of
falling O2 sign (rising pCO2/ Falling pO2),
Ventilator Free Breathing response
- higher cervical lesion = ventilation
(canula or neck vent) -> reduce
- currently giving exercise then ventilation
is just removed, there may be a sign that
they need a ventilation such as increase
respiratory rate, decrease vital capacity,
decrease O2 sat
- VFB response: increase respiratory rate,
decrease O2 sat and vital capacity
- normal O2 sat: >95
- during exercise: <93 or 92
- poor tolerance of VFB: <89
- develops gradually
- have to notify the attending physician or
nurse in charge for urgent intubation and
ventilation
- goal: prevent pneumonia and atelectasis
- atelectasis: lung collapsed, common in
bed ridden
- pneumonia: weakness of diaphragm and
chest wall muscle it leads to impair the
clearance of secretion and ineffective
cough
- provide intervention and prevention for
these
- teach them coughing techniques
o DVT Pulmonary embolism
- 50-100% of untreated patient within 3-
14 days
- prolonged inactivity
- any level or ASIA grade you are still at
risk of DVT
- all of the SCI patients are subject to
prophylactic treatment
- for first 3 months they have to intake
heparin
- dislodged thrombus = pulmonary
embolism or stroke
- receive clearance to have ROM exercises
to LE, UE can exercise
- SSx: swelling on calf area, high
temperature on the area, reddening or
darkening of the skin, warmth on popliteal
or calf area, pain
- pulmonary embolism ssx: shortness of
breath, chest pain, painful when inhaling
I. CHRONIC COMPLICATIONS
1. Life expectancy
• High NL severity older age
- Higher neurologic level of injury and
older age = negative impact with regards
of the survival
- C4 level + severe + complete SCI + Older
age
• Respiratory > Cardiovascular
- Respiratory common cause of death after
SCI more than the cardiovascular
- pneumonia/ pulmonary embolism
- cardiovascular: heart attack, Myocardial
Infarction
• Increase risk of suicide
• Reduced among survivors of SCI
• Mortality rate are high in their 1st year
having SCI
• Survived 1 year after SCI life expectancy is
approximately 90% of normal
2. Cardiovascular complications
• Autonomic dysreflexia
- can be seen in chronic SCI, above T6
affectation
- exaggerated sympathetic response
towards a noxious stimulus
- seen in cervical and thoracic lesion of SCI
o Clinical manifestations
o Triggering factors
- noxious stimuli such as: pain
from bladder distention,
constipation or pressure sores
- if TF is not present, patient may
be having a heart attack
o Management of acute attacks
- Monitor BP
- sit the patient upright to lower
BP
- loosen-tight fitting garments
- correct noxious stimuli
o Medications
- Nifedipine (10mg oral)
- Hydralazine (10mg IV)
- Labetalol (10mg IV)
- Nitrates* (do not take if patient
is taking sildenafil = severe
hypotension), sildenafil is used
for erect dysfunction
3. Coronary artery disease (CAD)
• Increase risk d/t decrease muscle mass =
binawian ng fats
• Increase mortality rate (3x than gen pop)
- most common cause of death in
Philippines
• Atypical presentations of heart attack
- Autonomic Dysreflexia happens
- change in spasticity
 • PT Concern?
o EBP:
- Cardiorespiratory fitness:
(Moderate to vigorous intensity)
- Aerobics x 20 mins, 2x/wk
- Strengthening x3 sets, 2x/ wk
- Cardiometabolic benefit:
(moderate to vigorous intensity)
- Aerobics x 30 mins x 3x/ wk
- to prevent cardiovascular dse.
Use this
4. Cardiovascular homeostasis
• If NLI is above T6 level
- difficulty maintaining cardiovascular
homeostasis
- baseline bp: decreased
- baseline heart rate is decreased
- 50-60 bpm
- they could have hemodynamic
- they could have poor exercise intolerance
- submaximal -> moderate to vigorous
intensity
• Orthostatic hypotension (First several
months of SCI)
- gradual position changes
- compression stockings
- abdominal binders
• Cardiac arrythmia for acute cervical SCI
- incomplete: less frequent in chronic SCI
- complete: chronic or acute can possibly
have cardiac arrythmia anytime
- complete SCI life expectancy is short
II. PULMONARY COMPLICATIONS
- seen in high and cervical thoracic SCI because of
respiratory muscles
- we want to prevent atelectasis and pneumonia
1. Pneumonia
2. Ventilatory failure
- signs: increase RR, decrease Force Vital Capacity,
decrease PO2
3. DVT pulmonary embolism
4. Dyspnea and exercise intolerance
III. URINARY COMPLICATIONS
A. Bladder dysfunction or neurogenic bladder
• Bladder/ Detrusor hyperactivity
- reflexive bladder = empty even though it is not yet
full
- decrease capacity of bladder over time
- smooth muscle = prone to bladder spasm
• Sphincter hyperactivity
- cannot store urine when the sphincter is reflexive
- problem in emptying the bladder
- hyperactive = most of the time it is active
• Detrusor sphincter dyssynergia
- not in synch
- bladder is trying to empty, sphincter closes
- miscommunication between bladder and
sphincter
- relaxed sphincter = about to expel the urine
- cannot empty bladder if the sphincter is close
- problem in dyssynergia: elevate the bladder
pressure and vesico (bladder) ureteral (ureter)
reflux (urine from the bladder)
• Bladder flaccidity
- produced in LMNL
- cauda equina syndrome wherein the tail of spinal
cord had injury
- does not contract
- problem is difficulty in emptying bladder
- CIC or Clean Intermittent Catheterization =
perform bladder emptying every 4 hrs
- target would be the bladder volume should be less
than 500mL
- max 2L per day for SCI patients
B. UTI
- most common
- twice per patient per year
- vesico ureteral reflux
- no private nurse = implement CIC
C. Urinary calculi
- kidney stone = usually they have increase limb
spasticity and autonomic dysreflexia
- could be heart attack or kidney stones
- emergency response is needed
D. Vesicoureteral reflux (VUR)
- high bladder function and recurrent UTI
- could lead to renal insufficiency
E. Renal insufficiency
- giving up of kidneys = dialysis
- risk: cumulative incident of certain urinary
complication
- anticipated 20-30 years after SCI
IV. MUSCULOSKELETAL COMPLICATIONS
A. Contractures (High level lesion)
- develops around 3 months of persistent position
- not all contractures are bad
• Positioning
- hip = minimize flexion of hip and knee
- elbow = minimize flexion
- knee
- ankle = do not plantarflex all the time
- shoulder = minimize adduction and internal
rotation
- use of wheelchair, maintain the lumbar lordosis
• ROM SCI because body is not yet aware what
- to prevent developing contracture has happened/ bone fragility
• Splinting - two years post- SCI there’s a new steady
- if patient cannot be supervised overtime state level between bone resorption and
• Facilitate function formation/ normalize
- C6 myotome - a lot of resorption of bone but lesser
- tenodesis effect wants to preserve by the doctor formation of bone
- flexion of wrist and extension of finger = tenodesis • Management
effect - Bisphosphonates to attenuate bone loss
- slight elbow flexion contracture can improve the - side effects of Bisphosphonates:
weakened biceps muscle (15-20 deg) a. Vertigo
B. Pressure ulcers b. Femoral fracture (prolonged use)
- bed ridden: c. Upper GI effects
• Ischium (31%) - has gastric irritation/ heart burn
• Sacrum (18%) • FES or Functional Electrical Stimulation
• Malleolus (4%) - minimal effectiveness in bone density
• Trochanter (26%) - with exercise = better outcome
• Heel (5%) • Heterotopic ossification
• Feet (2%) - found at the large joints below
- Wheelchair pressure ulcers: Neurological Level of Injury usually
• Ischial tuberosity affected (e.g., hip)
• Heel - bony formation in the soft tissue because
of osteogenic cells that is inactive in soft
• Greater trochanter (but lesser risk)
tissues
• Back of the knee/ popliteal fossa
- physically inactive = they are the one who
• Scapula
activates
• Elbows
- first 12 weeks after SCI for about 50%
• Back rest should be up to the inferior angle of
- symptoms: decreased ROM, end feel
scapula at the level of T7
would be bony, inflammatory symptom
• Preventive strategies:
such as swelling, redness, warmness in the
- should be check regularly
area
1. Examine
• DDx: DVT, Cellulitis, infection, hematoma
- skin over the areas such as skin over bony
and tumor
prominences, skin that are prone to shear and
o Test
friction
- triple phase bone scan (most
2. Apply
reliable)
- emollient or moisturizers daily to reduce
- elevated serum alkaline
friction
phosphatase (Early)
3. Teach
- radiograph (late/ least reliable)
- the patient with upper body strength to do
o Medication
pressure releases throughout the day
- etidronate
- ex: supine to sidelying
- side Effects: bone/ joint/ muscle
- wheelchair: increase strength in latissimus
pain, bone fracture
dorsi to carry weight and de-load a certain
- taken for 10 weeks
body parts
D. Spasticity
- changing of position in wheel chair every 15
• Negative effects
mins
- complain of pain, contracture, spasm
- bed ridden patient should change position
- interfere with sleep
every 2hrs
- decreased ROM, affects ADLs
4. Maintain
• Positive effects
- maintenance of adequate nutritional intake
- increase tone may facilitate some
and weight
functional activities including standing
- heavier = difficult to change position
and transfers
C. Bone metabolism
- spastic g.max and quads = helps patient
• Osteoporosis
to stand
- increase bone resorption 1st week post-
 - promote venous return
- helps minimize DVT
- lesser edema
- lesser incident of orthostatic
hypotension
• Medication S/E:
- sedation, dry mouth, dizziness, and
weakness
- strengthening exercise is not reliable
- patient may not process all of the
information you say
- prone to falls
E. Repetitive overuse injuries
- Shoulders > wrist > hand > elbow

V. NEUROLOGIC DETERIORATION
- less frequent
• Syringomyelia
- development of fluid filled cyst in spinal cord
- Sx: worsening motor, sensory, bowel and bladder
density
- challenge: ability when to refer the patient back to
the physician
• Progressive post myelomalacic myelopathy
- adhesion formation and cord tethering
- like syringomyelia but there’s no bowel and
bladder dysfunction
- Sx: increase spasticity, worsening motor, sensory

VI. PAIN SYNDROMES

- back to patient’s physician for medication as they
develop certain pain
- 2/3 has severe pain that affects their quality of life

VII. OTHER COMPLICATIONS

FUNCTIONAL DEFICITS 1. GI complications
- refer to practiced physician
2. Sexual dysfunction
3. Thermoregulatory dysfunction
- hyperthermia during exercise
- problem: not that reliable especially from caudal
to NLI as they may have a fever but temperature is
cold
4. Psychiatric complications
PROGNOSIS
- around 4-20%
- to predict patient’s survival: depends on the age, SCI
injury and ASIA grade
LEVEL OF INJURY
- higher lesion = worse the prognosis
• C1-C3
- high level of SCI
- 6x increase risk of death
 • C4-C5 - Arteriosclerosis,dissecti
- 2.5x increase risk of death on,FMD
• C6-C8 - Superimposed
- 1.5x increase risk of death thrombosis
● Embolism
○ Arterial obstruction from debris
IMPAIRMENT SCALE from another source
• Complete <incomplete injury ● Lacunar Stroke
• With < without significant comorbidity ○ minute ischemia of perforating
GRADE % OF PTS AMBULATORY
arteries
● Systemic Hypoperfusion
A <10% At one year
○ Circulatory collapse
B 40% 54% becomes grade C/D
○ Multiorgan involvement
C 62%
D 97% THROMBOSIS
● Large Vessel Disease
SUMMARY OF CLASS ○ Common & Internal Carotids
○ Circle of Willis & proximal branches
• Examination and Evaluation
● Small Vessel Disease
• Complications
○ Penetrating arteries
• Referral
○ “Lacunar Stroke”
- Stenosis hardening or primary
thrombosis of small arteries
● “Stuttering” course
- Small symptoms that can be severe

NOTE: Thrombotic stroke recovery is longer than

embolic stroke
CEREBROVASCULAR DISORDER
EMBOLISM
● Disorders of neurologic system upper motor - Dislodge then it goes to brain
neuron lesion caused by any vascular - Heart
disturbances ● Cardiac
● AKA stroke ○ Atrial fibrillation
○ Heart valves, atrial thrombus, recent MI,
STROKE dilated CM, endocarditis, recent CABG
● A clinical syndrome characterized by rapidly ● Aortic
developing clinical symptoms and/or signs of ● Arterial (e.g. carotids)
focal, and at times global (applied to patients in ● Other/Unknown
deep coma and those with subarachnoid ○ DVT- “Paradoxical embolus”
haemorrhage), loss of cerebral function, with ● Abrupt onset, rapid improvement
symptoms lasting more than 24 hours, or ● Onset: Sudden, Seizure, Slurring, Siallorhea,
leading to death, with no apparent cause other
than that of vascular origin. HYPOPERFUSION
● Hatano 1976 ● Shock
○ Cardiogenic, Septic, Hypovolemic (low
CLASSIFICATION blood volume)
● Pathologic ● Sx are more diffuse/nonfocal
● temporal - Global in nature
● Artery affected ● “Border-zone regions”
1. Ischemic stroke - Transverses from frontal to temporal
● Thrombosis lobe or whole parieto fronto-temporal
○ Aka In situ arterial obstruction ○ Cortical blindness
○ Stupor
 ○ Proximal Weakness
2. Hemorrhagic stroke
- Pumutok na blood vessel
- Types of hemorrhages: intracranial,
subarachnoid (dangerous), subdural
(Common), epidural
● Intracerebral Hemorrhage (ICH)
○ Bleeding within the brain tissue
○ Hard to handle
○ Forms a hematoma (necrotic
tissue)
○ Growth stopped by tamponade
or leaking into the ventricles or
CSF
○ SSx: Headache, vomiting,
delirium, stuporous
○ Progressive sx
● Subarachnoid Hemorrhage (SAH)
○ Bleeding into CSF on outer
aspect of brain
○ Thunder clap headache
○ Quick rise in ICP
○ Sudden onset headache in 97%
○ Aneurysm & AVMs are most
common cause
○ More sudden
○ Sudden loss of motor function in DIFFERENT PATHOGENESIS OF STROKE
one side of the body completely Criteria Thromb Emboli Lacunar Hemorr
otic c hagic
CAUSES OF ICH
● HTN
Inciden 40% 30% 20% 10%
● Trauma ce
● Bleeding Disorder
● Inherited
● Acquired, i.e. meds Mechan Atheros Choles Atherosc Hyperte
ism clerotic torol lerotic nsion
● Amyloid
● Drug use
● Cocaine Onset Gradual Abrupt Chronic Sudden
● Amphetamines and process
progres
● AVMs
sion
● Bleeding into tumor
● Vasculitis Scenari (+) After
o warning MI
signs

Sites ICA/MC Cortica Small Sites of

A l small perforati lacunes
vessel ng
s arteriole
s
 Clinical Aphasia Cortica Discrete Inc ICP
Manifes Visual l & Subcort ABCDs OF TIAs
tation field deficits specific ical/ ● Prediction of risk of stroke
cuts subcortic cortical
● Age >60 = 1 pt
Hemipa al deficits
resis, deficits ● Blood Pressure >140/90 = 1
hemise ● Clinical Features
msory ○ Unilateral weakness = 2
○ Isolated speech deficit = 1
○ Other = 0
TEMPORAL CLASSIFICATION
● Duration
● Complete stroke
○ >60 minutes = 2
- Had stroke but Does not resolve for 24
○ 10-59 minutes = 1
hrs and the patient is stable for 3-7 days
○ <10 minutes = 0
● Reversible Ischemic Neurological Deficit
- This is a transient neurological event
that lasts longer than 24 hours.
● Stroke in Evolution
- This denotes an unstable ischemic
event characterized by progressive
development of more severe
neurological impairment, and is often
associated with active occlusive
thrombosis of a major cerebral artery.
- Does not stabilize for 24 hrs and ● Deteriorating Stroke
progresses for more than 24 hrs up until - This is used to refer to the patient
72 hrs whose neurological status is
● Transient Ischemic Attack (TIA) deteriorating after admission to the
- Refers to the temporary interruption of hospital.
blood supply to the brain. Symptoms of - Slow progression
focal neurological deficit may last for - Ending: death
only a few minutes or for several hours, ● Young Stroke
but do not last more than 24 hours. After - This is used to describe a stroke
the attack is over there is no evidence of affecting persons below the age of 45
residual brain damage or permanent
neurological dysfunction. STROKE SYNDROMES
- Fully recovered after 24 hrs
- Aka mild stroke CAUSES OF STROKE IN CHILDREN AND YOUNG
- Higher risk of complete stroke for 6 ADULTS
months to 1 year ● Cerebral embolism
● Trauma to extracranial arteries
○ Thromboembolic occlusion
○ Dissection
● Subarachnoid hemorrhage
○ Aneurysm
RISK OF STROKE POST- TIA ○ Arteriovenous Malformation
● NASCET trial suggested 90-day stroke risk of ● Vasculopathy
20% with non-retinal TIAs (higher than for true ● Coagulopathy
stroke) ● Homocystinuria
● 2000 JAMA study ● Oral contraceptives
○ 5% risk w/in 2 days ● Post-partum
○ 11% risk w/in 90 days ● Drug-induced
○ Higher risk with age >60, DM, sx >10
min, weakness, speech impairment ISCHEMIC PENUMBRA
● 2004 Neurology study: 21% risk of
stroke/MI/death within 1 year of TIA
 ● Complete cerebral circulatory arrest results in ● Watershed Areas: overlap between major
irreversible cellular damage with a core of area arteries
of focal infarction within damage.
● The ischemic penumbra consist of viable but
metabolically lethargic cells.
● There is a release of neurotransmitters
(glutamate and aspartate)
● Larger the ischemia, larger ischemic penumbra
● Attributes brain into cerebral shock

Right Hemiplegia Left Hemiplegia

(Left Hemisphere) (Right Hemisphere)
Visuomotor perception and Visuomotor perceptual
memory intact impairment

Visual Learning Loss of Visual Memory

Learning is step by step, Left sided neglect;

encourage imitation impulsive or unorganized
activities of daily living

Unable to communicate Safety problem with many

effectively vocabulary and falls
auditory span reduced Inability to follow through

Able to pickup ideas Does not learn from

through body mistakes or observing
language,facial expression others

Cautious and unorganized Learning is impaired;

when approaching an persons performance may
unfamiliar situation not improve ACA STROKE
Signs and Symptoms Structure Involved
Learns from mistakes able Often battles with staff or
to synthesize parts of a premature discharge
task Contralateral hemiparesis Primary motor area, medial
involving mainly the LE aspect of cortex, internal
(UE is more spared) capsule

ANTERIOR VS POSTERIOR AFFECTATION

● Anterior Contralateral hemiparesis Primary sensory area,
○ Hemiparesis involving mainly the LE medial aspect of cortex,
(UE is more spared)
○ Hemianesthesia
○ Aphasia
Urinary incontinence Posteromedial aspect of
○ Dysarthria
superior frontal gyrus
○ Headache
○ Mono-ocular blindness
Problems with imitation Corpus callosum
○ Facial weakness and bimanual tasks,
○ Eye deviation apraxia
● Posterior
○ Dysarthria
○ Dysphagia Abulia (akinetic mutism), Uncertain localization
○ Diplopia slowness, delay, lack of
○ Dizziness spontaneity, motor inaction

○ Facial weakness
○ Eye deviation toward flexion Contralateral grasp reflex, Uncertain localization
sucking reflex
CORTICAL BLOOD SUPPLY
● ACA: Medial Frontal Perfusion ● Anterior cerebral artery
● MCA: Lateral Perfusion - Contralateral hemiparesis (distal leg
● PCA: Posterior medial Perfusion, cerebellum more than arm)
 -Contralateral sensory loss (distal leg - Left hemisphere = wernicke’s aphasia
more than arm) - Horizontal gaze palsy
- Urinary incontinence - Language and cognitive deficits in the
- Left-sided ideomotor apraxia or tactile left hemisphere:
anomia ■ Aphasia (motor, sensory, global)
- Severe behavior disturbance (apathy or ■ apraxia (ideomotor and
“abulia,” motor inertia, akinetic mutism, ideational)
suck and grasp reflexes, and diffuse ■ Gerstmann syndrome (agraphia,
rigidity—“gegenhalten”) acalculia, left–right confusion,
- Eye deviation toward side of infarction and finger agnosia)
- Reduction in spontaneous speech, - Language and cognitive deficits in the
perseveration right hemisphere: constructional/spatial
● Most common characteristic defects (constructional apraxia, or
○ contralateral hemiparesis apractognosia, dressing apraxia);
- Greater involvement of LE agnosias (atopognosia, prosopagnosia,
anosognosia, asomatognosia); left-sided
MCA STROKE unilateral neglect; amusia.
Signs and Symptoms Structure Involved
Signs and Symptoms Structure Involved

Contralateral hemiparesis Primary motor area and internal

involving mainly the UE capsule Limb-Kinetic Apraxia Premotor or parietal cortex
and Face

Contralateral hemisensory Primary sensory area and Contralateral homonymous Optic radiation in internal
loss involving mainly the internal capsule hemianopsia capsule
UE and the face

Receptive speech Wernicke’s cortical area Loss of conjugate gaze to Frontal eye fields or their
impairment: Wernicke’s or (posterior portion of the the opposite side descending tracts
fluent aphasia with temporal gyrus) in the dominant
impaired auditory hemisphere, typically the left.
comprehension and fluent Ataxia of contralateral limb Parietal lobe
speech with normal rate (s)
and melody
Pure motor hemiplegia Upper portion of posterior
Global aphasia: nonfluent Both third frontal convolution
(lacunar stroke) limb of internal capsule.
speech with poor and posterior portion of the
comprehension superior temporal gyrus.

Perceptual deficits; Parietal sensory association ● Superior division

unilateral neglect, depth cortex in the nondominant ● Inferior division stroke
perception, spatial hemisphere, typically the right.
● Occlusion at the bifurcation or trifurcation of the
relations, agnosia.
middle cerebral artery
● Occlusion of the stem of the middle cerebral
artery
● Superior division stroke
- results in contralateral hemiparesis that
affects the face, hand, and arm but
spares the leg; contralateral
hemisensory deficit in the same
distribution; but no homonymous
● Middle cerebral artery
hemianopia. If the dominant hemisphere
- Contralateral hemiplegia (face and arm
is involved, these features are combined
greater than leg)
with Broca's (expressive) aphasia, which
- Lower quadrant paresis of the face
is characterized by impairment of
- Contralateral hemisensory deficit (face
language expression with intact
and arm greater than leg)
comprehension.
- Homonymous hemianopsia
● Inferior division stroke ● Most common characteristic
- is less common in isolation and results ○ contralateral spastic hemiparesis and
in contralateral homonymous sensory loss of the face, upper extremity
hemianopia that may be denser (UE), and lower extremity (LE)
inferiorly; marked impairment of cortical - face and UE more involved than
sensory functions, such as the LE
graphesthesia and stereognosis on the
contralateral side of the body; and PCA STROKE
disorders of spatial thought, including a Signs and Symptoms Structure Involved
lack of awareness that a deficit exists
(anosognosia), neglect of and failure to
Contralateral homonymous Primary visual cortex or optic
recognize the contralateral limbs,
hemianopsia radiation
neglect of the contralateral side of
external space, dressing apraxia, and
Visual agnosia Left occipital lobe
constructional apraxia. If the dominant
hemisphere is involved, Wernicke's
(receptive) aphasia occurs and is Prosopagnosia: hard time Visual association cortex
naming people, no facial
manifested by impaired comprehension recognition
and fluent but often nonsensical speech.
With involvement of the nondominant Dyslexia (difficulty reading) Dominant calcarine lesion and
without agraphia (difficulty posterior part of corpus
hemisphere, an acute confusional state
writing), color (anomia), callosum
may occur. and color discrimination
● Occlusion at the bifurcation or trifurcation of problems
the middle cerebral artery
- involves a lesion situated at the point Memory defect Lesion of inferomedial portions
where the artery splits into two (superior of temporal lobe or bilaterally or
and inferior) or three (superior, middle, on the dominant side only.
and inferior) major divisions. This severe
stroke syndrome combines the features Topographic disorientation Nondominant primary visual
of superior and inferior division stroke. area, usually bilaterally.
- Its clinical features include contralateral
hemiparesis and hemisensory deficit
● Contralateral homonymous hemianopia or
involving the face and arm far more than
quadrantanopia
the leg; homonymous hemianopia; and,
● Memory disturbance with bilateral inferior
if the dominant hemisphere is affected,
temporal lobe involvement
global (combined expressive and
● Optokinetic nystagmus, visual perseveration
receptive) aphasia.
(palinopsia: anywhere she see there’s constant
image), hallucinations in the blind field
● There may be alexia (without aphasia or
● Occlusion of the stem of the middle cerebral
agraphia), and anomia for colors, in dominant
artery
hemisphere involvement
- occurs proximal to the origin of the
● Cortical blindness, with patient not recognizing
lenticulostriate branches. Because the
or admitting the loss of vision (Anton’s
entire territory of the artery is affected,
syndrome), with or without macular sparing,
this is the most devastating of middle
poor eye–hand coordination, metamorphopsia,
cerebral artery strokes. The resulting
and visual agnosia when cortical infarction is
clinical syndrome is similar to that seen
bilateral
following occlusion at the trifurcation
● Pure sensory stroke: may leave anesthesia
except that, in addition, infarction of
dolorosa with “spontaneous pain,” in cortical and
motor fibers in the internal capsule
thalamic ischemia
causes paralysis of the contralateral leg.
● Contralateral hemiballism and choreoathetosis
The result is a contralateral hemiplegia
in subthalamic nucleus involvement
and sensory loss affecting the face,
● Oculomotor palsy, internuclear ophthalmoplegia,
hand, arm, and leg.
loss of vertical gaze, convergence spasm, lid
 retraction (Collier’s sign), corectopia - Alloesthesia: a noxious stimulus on the side of
(eccentrically positioned pupils), and sometimes the hemisensory disturbance is perceived at the
lethargy and coma with midbrain involvement corresponding area of the other (normal) side

HEMORRHAGIC STROKES (Global Affectation) Thalamic hemorrhage

1. Frontal lobe – Hemisensory deficit and, to a lesser degree,
- Abuli hemiparesis
- Contralateral hemiparesis – Anomic aphasia with impaired comprehension, with
- Bifrontal headache (maximum lesions of the dominant thalamus
ipsilateral) – Convergence–retraction nystagmoid movements,
- Occasionally, mild gaze preference impairment of vertical gaze, and pupillary near light
away from the hemiparesis dissociation
- Have UE and LE affectations – Downward–inward deviation of the eyes
- Conduction aphasia – Unilateral or bilateral pseudo-sixth nerve paresis
– Skew deviation
Parietal lobe – Conjugate gaze palsy to the side of the lesion
– Contralateral hemisensory loss (wrong side) or conjugate horizontal gaze deviation
– Neglect of the contralateral visual field
– Headache (usually anterior temporal location) Cerebellar hemorrhage
– Mild hemiparesis Most common in the area of the dentate nucleus
– Occasionally, hemianopia or anosognosia Symptoms:
- Broca's Aphasia – Sudden occipital headache
- Transcortical Motor – Nausea and repeated vomiting
- Transcortical Mixed – Dizziness, vertigo
- Transcortical Sensory – Inability to stand
– Variable degrees of alertness
Temporal lobe – Small reactive pupils
– Wernicke’s aphasia (dominant temporal lobe) – Skew deviation
– Conduction or global aphasia (dominant temporal – Ipsilateral gaze palsy
parietal lobe) – Ocular bobbing and nystagmus toward the gaze;
– Variable degrees of visual field deficit paresis
– Headache around or anterior to ipsilateral ear – Ipsilateral peripheral facial weakness
– Occasionally, agitated delirium – Ipsilateral absence or decrease of corneal reflex
- If dominant part (Global Aphasia) – Slurred speech
– Gait or truncal ataxia
Occipital lobe – Bilateral hyperreflexia and Babinski signs
– Ipsilateral orbital pain
– Contralateral homonymous hemianopia
- Various visual affectations
Pontine hemorrhage
Putaminal hemorrhage - Symptoms: Headache, vomiting, vertigo, dysarthria,
- The putamen is the most common site of Sudden loss of consciousness, often progressing
hypertensive ICH into deep coma
- Hemiparesis or hemiplegia and, to a lesser
degree, hemisensory deficit Findings
- Transient global aphasia with dominant – Sudden-onset coma
hemispheric lesions – Quadriparesis, quadriplegia
- Agnosia or unilateral neglect with nondominant – Respiratory abnormalities
hemispheric lesions – Hyperthermia
- Homonymous hemianopia – Pinpoint reactive pupils
- Contralateral gaze palsy: the patient looks – Eyes fixed in a central position
toward the hematoma and away from the – Loss of brain stem reflexes, including the
hemiplegia oculocephalic (doll’s head) and the oculovestibular
reflexes
– Ocular bobbing
LACUNAR STROKES
1. Pure motor hemiparesis—This consists of
hemiparesis affecting the face, arm, and leg to a roughly
equal extent, without an associated disturbance of
sensation,
vision, or language. When lacunar in origin, it is usually
due to a lesion in the contralateral internal capsule or
pons. Pure motor hemiparesis may also be caused by
internal carotid or middle cerebral artery occlusion,
subdural hematoma, or intracerebral mass lesions.
2. Pure sensory stroke—This is characterized by
hemisensory loss, which may be associated with
paresthesia, and results from lacunar infarction in the
contralateral thalamus. It may be mimicked by occlusion
of the posterior cerebral artery or by a small hemorrhage
in the thalamus or midbrain.
3. Ataxic hemiparesis—In this syndrome, sometimes
called ipsilateral ataxia and crural (leg) paresis, pure
motor hemiparesis is combined with ataxia of the
hemiparetic side and usually predominantly affects the
leg. Symptoms result from a lesion in the contralateral
pons, internal capsule, or subcortical white matter.
4. Dysarthria-clumsy hand syndrome—This consists
of dysarthria, facial weakness, dysphagia, and mild
weakness and clumsiness of the hand on the side of
facial
involvement. When the syndrome is caused by a lacunar
infarct, the lesion is in the contralateral pons or internal
capsule. Infarcts or small intracerebral hemorrhages
at a variety of locations can produce a similar syndrome,
however. In contrast to the lacunar syndromes described
above, premonitory TIAs are unusual.
BRAINSTEM STROKES
Midbrain
Weber’s syndrome
Ventral midbrain
CN III
Corticospinal tract
Ipsilateral CN III palsy, including parasympathetic
paresis (i.e., dilated pupil)
Contralateral hemiplegia
Benedict’s syndrome
- Ipsilateral CN III palsy, usually with a dilated pupil
- Contralateral involuntary movements (intention tremor,
hemichorea, or hemiathetosis)
Benedict syndrome:
a) red nucleus (contralateral involuntary movements,
including intention tremor,
hemichorea, and hemiathetosis;
b) brachium conjuctivum (ipsilateral ataxia);
c) parasympathetic root fibres of CN III (ipsilateral
oculomotor paresis with fixed and dilated pupil
Claude’s syndrome
- Ipsilateral CN III palsy, usually with a dilated pupil
- Prominent cerebellar signs
- Contralateral involuntary movements (intentional
tremor, hemiataxia, and no hemiballismus)
- Claude syndrome:
a) dorsal red nucleus (contralateral involuntary
movements, including intention tremor, hemichorea, and
hemiathetosis;
b) brachium conjunctivum (prominent cerebellar signs
and no hemiballismus);
c) dorsal midbrain tegmentum
Parinaud syndrome
• Paralysis of conjugate upward (and
occasionally downward) gaze
• Pupillary abnormalities (dissociation of pupil
response close to light)
• Convergence–retraction nystagmus on
upward gaze
• Pathological lid retraction (Collier’s sign)
• Lid lag
• Pseudo-abducens palsy
• a) superior colliculi (conjugated gaze
paralysis upward);
• b) medial longitudinal fasciculus (nystagmus
and internal ophthalmoplegia);
• c) eventual paresis of the CNs III and IV; d)
cerebral aqueduct stenosis/obstruction
(hydrocephalus).
• Involvement of the inferior colliculi produces
hearing loss.
PONTINE LESIONS
Raymond–Cestan syndrome
• Cerebellar signs (ataxia)
• Contralateral reduction of all sensory
modalities (face and extremities)
• Contralateral hemiparesis
• a) superior cerebellar peduncle (Cerebellar
ataxia with a course “rubral” tremor);
 • b) medial lemniscus and spinothalamic tract
(contralateral decrease in all sensory
modalities, involving face and extremities).
Ventral extension of the lesion involves
additionally;
• c) corticospinal tract (contralateral
hemiparesis)
• d) paramedian pontine reticular formation
(Paralysis of the conjugate gaze towards the
side of the lesion).
Marie–Foix syndrome
• Ipsilateral cerebellar ataxia
• Contralateral hemiparesis
• Variable contralateral hemihypesthesia for
pain and temperature
• Lateral pontine lesions(especially brachium
pontis)
• a) superior and middle cerebellar peduncles
(ispilateral cerebellar ataxia);
• b) corticospinal tract (contralateral
hemiparesis);
• c) spinothalamic tract (variable contralateral
hemihypesthesia for pain and temperature).
Foville’s syndrome
• Contralateral hemiplegia (with facial
sparing)
• Ipsilateral peripheral-type facial palsy
(involvement of CN VII fascicles)
• Gaze palsy to side of lesion
• Contralateral hemiplegia (with facial
sparing)
• Ipsilateral peripheral-type facial palsy
(involvement of CN VII fascicles)
• Gaze palsy to side of lesion
Millard–Gublar syndrome
• Contralateral hemiplegia (sparing the face)
• Ipsilateral lateral rectus palsywith diplopia
• Ipsilateral peripheral facial paresis
Ventral paramedian pons ! CN VI and VII
fascicles ! Corticospinal tract
• Millard–Gubler syndrome: a) pyramidal tract
• (contralateral hemiplegia sparing the face);
b) CN VI (diplopia accentuated when
• the patient “looks towards” the lesion); c)
CN VII (ipsilateral peripheral facial nerve
• paresis).
Locked-in syndrome (differentiation)
• Tetraplegia due to bilateral corticospinal
tract involvement
• Aphonia due to involvement of the
corticobulbar fibers destined for the
lower cranial nerves
• Occasionally, impairment of horizontal
eye movements due to bilateral
involvement of the fascicles of CN VI
• Locked-in syndrome: a) bilateral
corticospinal tracts in the basis pontis
(tetraplegia); b) corticobulbar fibres of
the lower CNs (aphonia); c) occasionally
• bilateral fascicles of the CN VI
(impairment of horizontal eye
movements).
Differential diagnosis in pontine lesions
Dysarthria–clumsyhand syndrome
• Clumsiness and paresis of the hand,
ipsilateral hyperreflexia,and Babinski
sign
• Facial weakness
• Severe dysarthria and dysphagia
Basis pontis (lacunar infarction) at junction of
upper onethird
and lower twothirds of pons! CN VII
Ataxic hemiparesis
• Hemiparesis more severe in the lower
extremity
• Ipsilateral hemiataxia
• Occasional dysarthria, nystagmus, and
paresthesias
• Lacunar infarction involving the basis pontis
at the junction
• of the upper third and lower twothirds of the
pons
MEDULLA LESIONS
Dejerine anterior bulbar syndrome
• Ipsilateral paresis, atrophy (tongue deviates
toward the lesion)
• Contralateral hemiplegia with sparing of the
face
• Contralateral loss of position and vibratory
sensation. Pain and temperature sensation
are spared
Medial medulla oblongata (corticospinal tract, • ! Lower pons (to the region of exit of CNs
medial lemniscus, CN XII) VII and VIII)
Medulla (caudal): Medial medullary (Dejerine)
INDIRECT IMPAIRMENTS
syndrome: a) CN XII (ipsilateral paresis atrophy,
Complications following a stroke
and fibrillation of the tongue; b) pyramidal tract
• Falls
(contralateral hemiplegia with sparing of the face);
• Musculoskeletal problems
c) medial lemniscus (contralateral loss of position
• Bowel & bladder problems
sense and vibration occasionally); d) medial
• Physiologic conditioning
longitudinal nystagmus (upbeat nystagmus).
• Associated medical problems
o HPN
Wallenberg’s syndrome
o Diabetes
• Ipsilateral facial hypalgesia and o IHD
thermoanesthesia o CHF
• Contralateral trunk and extremity hypalgesia • Venous thromboembolism
and thermoanesthesia • Skin breakdown
• Ipsilateral palatal, pharyngeal, and vocal • Deconditioning
cord paralysis with dysphagia and
dysarthria Common specific problems
• Ipsilateral Horner’s syndrome • Shoulder subluxation
• Vertigo, nausea, and vomiting • Types of slings
• Ipsilateral cerebellar signs and symptoms o Harris hemisling
• Occasionally, hiccups and diplopia o Forearm trough
o Overhead sling
Lateral medulla! Inferior cerebellum o Lapboard
(Inferior cerebellar peduncle, descending • Brachial plexus Injury
sympathetic tract, spinothalamic tract, CN V • Heterotropic Ossification
nucleus)
a) Nucleus and tract of CN V (ipsilateral facial pain EVALUATION OF STROKE
and hypalgesia and thermoanesthesia); History
b) spinothalamic tract (contralateral trunk and • History of:
extremity hypalgesia and thermoanesthesia); o HTN
c) nucleous ambiguus (ipsilateral palatal, o CAD
o DM
pharyngeal, and vocal cord paralysis with
o Previous TIA in same vascular
dysphagia and dysarthria); d) vestibular nuclei
distribution
(vertigo, nausea, and vomiting); e) descending
o Symptomatic deficits that wax and
sympathetic fibers (ipsilateral Horner’s syndrome); wan
f) inferior cerebellar peduncle and cerebellum o Gradual onset
(ipsilateral cerebellar signs and symptoms); g) • Suggests: atherosclerotic disease and
medullary respiratory centers (hiccups); h) lower thrombosis
pons (diplopia).
• History of
Lateral pontomedullary syndrome o A-Fib
• All clinical findings seen in the lateral o Valvular replacement
medullary syndrome o Recent MI
• Ipsilateral facial weakness o Multiple TIAs involving different
• Ipsilateral tinnitus and occasionally hearing vascular distributions
disturbance o Sudden onset of symptoms
• ! Lateral medulla • Suggests: Embolism
• ! Inferior cerebellum
• History of:
 o Recent neck injury-MVA, Sports
injury
o Chiropractic manipulation
• Suggests: Carotid dissection
• History of:
o Straining or coughing immediately
preceding symptoms
• Suggests: ruptured aneurysm
• History of:
o Sudden onset of symptoms
o Headache (minority of patients with
ischemic stroke)
• Suggests: Hemorrhagic stroke
This is a flow diagram to help you organise your
acute assessment of patients with suspected
stroke. It also includes a reminder about the
common stroke mimics.
We might want to consider more risky
treatments for really bad strokes.
Physical Exam
• Not inclusive, but some pointers:
o Signs of emboli- Janeway lesions,
Osler nodes
o Bleeding dyscrasia- ecchymosis,
petechiae
o Papilledema- mass lesion, HTN
crisis, cerebral vein thrombosis
o Carotid bruit or murmurs- vascular or
cardiac etiol.
Initial Evaluation: Physical Exam
• Vital signs
o Temperature, Pulse, Blood Pressure
• Pulses
• Carotid Bruit
• Cardiac Exam
• Funduscopic exam
• Skin exam
• Signs of trauma
Neurologic Exam
• Level of consciousness/GCS
• Language/Speech
• Cranial nerves
• Vertigo, diplopia, ataxia
• Visual deficits
• Weakness/Paralysis
• Reflexes/ Babinski
Glasgow Coma Scale
• Patients are awarded points based on eye
opening, best verbal response, and best
motor response. The patient's GCS score
can range from 3/15 to 15/15
• Eye opening score: 4, eyes open; 3, eyes
open to speech; 2, eyes open in response
to pain; 1, no eye opening
• Best verbal response score: 5, alert and
oriented; 4, confused; 3, responds with
inappropriate words; 2, makes
incomprehensible sounds; 1, no verbal
response
• Best motor response score: 6, obeys
commands; 5, localizes pain; 4, responds to
pain with normal flexion/withdrawal; 3,
responds to pain with abnormal flexion; 2,
extends in response to pain; 1, no response
to pain
 o Sensitivity much better after 24 hrs
for ischemic stroke
o Early signs (<6 hrs)
o May indicate worse prognosis

Initial Evaluation: Studies

• CBC with platelets
• Electrolytes, Bun, Cr
• Glucose Hyperdense within 6hrs = hemorrhage
• LFTs
• PT/PTT
• O2 Sat
• ECG
• Chest Xray
• ESR
• Blood Cultures
• ANA
• Tox screen
• Alcohol level
• Blood type & cross
• Urine/Serum HCG
• Hypercoagulability Profile

White areas = blood

Initial Evaluation: Imaging Center area = site of rupture
• CT Scan
o “R/O Bleed”
 Kinesthetic sensations
Spasticity assessment
Tardieu Scale
• MRI
o T1/T2 images, DWI
o Provides immediate evaluation of
ischemia
o Not available for emergency use in
many settings
Neurologic Outcome Measures
Nottingham Sensory Assessment
• Sitting position
• Demonstrated first before blindfolding
• Random application of stimulus
• Grading ( 9 = Not tested)
o Tactile and stereognosis – 0= absent;
1=impaired; 2 = normal
o kinesthetic sensations – 0=absent;
1=appreciation of movement; 2 = able to
mirror the movement; 3 =within 10 deg
of end postion
o 2 point disc – distance between 2 points
• Done repeatedly for comparisons
• Increase in scores imply improvement
• Good intra-rater but poor inter-rater reliability
Tactile sensations
o Light touch
o Pressure
o Pinprick
o Temperature
o Tactile localization
o Bilateral simultaneous touch
• Appreciation of movement
• Stereognosis
• 2-point discrimination
• Tardieu Scale
• Modified Ashworth Scale
• Done in 3 velocities
o V1 = as slow as possible
o V2 = speed falling under gravity
o V3 = speed faster than gravity
• Recorded as X/Y, wherein X refers to the
quality of response and Y refers to the angle
of the muscle response
• X responses
0 no resistance throughout the course
1 Slight resistance, no clear cut at a
precise angle
2 Clear catch, followed by release
3 Fatigable clonus (< 10secs when
maintaining pressure)
4 Fatigable clonus (> 10 secs when
maintaining pressure)
• Done repeatedly
• The higher the score, the greater the
spasticity
• Good content validity for stroke
• Coincides with stretch-induced EMG activity
• Differentiates spasticity from contracture
Modified Ashworth Scale
• Measures resistance of a joint following
a rapid passive stretch
• Original scale used 0-4
• Modified in 1987 with 0, 1, 1+,2,3,4
0. no increase in muscle tone
1. Slight increase in muscle tone, catch and
release, or min resistance at the end range
1+ slight inc in muscle tone, catch followed
by min resistance throughout the remainder
(less than half) of the movement
2. More marked inc in muscle tone through
most of the range but part is easily moved
3. Considerable inc in muscle tone, passive
movement difficult
4. Affected parts rigid in flexion or extension
Step Test
• Test of dynamic balance
 • Pt places foot on a 7.5cm block then
back to the floor
Clinical Grading Scales in Subarachnoid
Hemorrhage
Botterell scale
• Conscious, with or without signs of bleeding
in the subarachnoid space I
• Drowsy, without significant neurological
deficit II
• Drowsy, with significant neurological deficit
III
• Major neurological deficit, deteriorating, or
older with preexisting
• cerebrovascular disease IV
• Moribund or near-moribund, failing vital
centers, extensor rigidity V
Hunt–Hess scale
• Asymptomatic or mild headache I
• Moderate to severe headache, nuchal
rigidity, may have oculomotor palsy II
• Confusion, drowsiness, or mild focal signs
III
• Stupor or hemiparesis IV
• Coma, moribund appearance, and/or
extensor posture V
Glasgow Coma Scale
• Patients are awarded points based on eye
opening, best verbal response, and best
motor response. The patient's GCS score
can range from 3/15 to 15/15
• Eye opening score: 4, eyes open; 3, eyes
open to speech; 2, eyes open in response
to pain; 1, no eye opening
• Best verbal response score: 5, alert and
oriented; 4, confused; 3, responds with
inappropriate words; 2, makes
incomprehensible sounds; 1, no verbal
response
• Best motor response score: 6, obeys
commands; 5, localizes pain; 4, responds to
pain with normal flexion/withdrawal; 3,
responds to pain with abnormal flexion; 2,
extends in response to pain; 1, no response
to pain
World Federation of Neurologic Surgeons
(WFNS) scale
• Glasgow Coma Scale score 15:
– no headache or focal signs I
• Glasgow Coma Scale score 15:
– headache, nuchal rigidity, no focal signs II
• Glasgow Coma Scale score 13–14:
– may have headache, nuchal rigidity, no focal
signs III
• Glasgow Coma Scale score 13–14:
– may have headache, nuchal rigidity, or focal
signs IVa
• Glasgow Coma Scale score 9–12:
– may have headache, nuchal rigidity, or focal
signs IVb
• Glasgow Coma Scale score 8 or less:
– may have headaches, nuchal rigidity, or focal
signs V
IVa to V candidate for surgery
Cooperative Aneurysm Study scale
• Symptom-free I
• Mildly ill- II , alert and responsive, headache
present
• Moderately ill - III
– Lethargic, headache, no focal signs
– Alert, focal signs present
• Severely ill - IV
– Stuporous, no focal signs
– Drowsy, major focal signs present IV
PHARMACEUTIC INTERVENTION
Acute Interventions & Management
Learning Objectives
Upon completion, participants will be able to:
• State the goal of managing patients with
medications following a transient ischemic
attack (TIA) or minor stroke
• Teach patients about their medications and
the importance of medication adherence
• Practice according to the Canadian Best
Practice Recommendations for Stroke Care
as they relate to interventional & medication
management
Implement Interventions
Canadian Best Practice Recommendations for
Stroke Care, 2008
• 3.2. Acute management of TIA and minor
stroke
 o Patients who present with symptoms
suggestive of minor stroke or TIA
must undergo a comprehensive
evaluation to confirm the diagnosis
and begin treatment to reduce the
risk of major stroke as soon as it is
appropriate to the clinical situation.
The Canadian Best Practice Recommendations for
Stroke Care 2008 stress the importance of a
comprehensive assessment to make an accurate
diagnosis and the timely initiation of treatment for
the patient who presents with symptoms suggestive
of a minor stroke or TIA. The ultimate goal is the
reducing the risk of a major stroke event.
Source: Lindsay P, Bayley M, Hellings C, et al;
Canadian Stroke Strategy Best Practices and
Standards Writing Group on behalf of the
Canadian Stroke Strategy, a joint initiative of
the Canadian Stroke Network and the Heart and
Stroke Foundation of Canada. Canadian Best
Practice Recommendations for Stroke Care
(updated 2008). CMAJ 2008;179:E1-E93
Implement Interventions
Medication Management
• Antihypertensives
o ACEI (Angiotensin Converting
enzyme)
o ARB (Angiotensin Receptor Blocker)
o Diuretics
o Calcium Channel Blockers
• Lipid lowering agents
o Statins
• Antithrombotic
o Antiplatelet
o Anticoagulant (Atrial fibrillation)
• Optimize diabetes management
Interventional Procedures
• Carotid Stenosis
o Carotid Endarterectomy
o Carotid Artery Stenting
Medication Management
• Goals of managing patients with
medications following a TIA or minor stroke:
o Minimize plaque formation
o Stabilize existing plaque
o Lowering risk of emboli in
appropriate individuals
• Medications include:
o Antihypertensive
o Statin
o Antithrombotic
• The goal of medical management in stroke
prevention is to minimize plaque formation
and inflammation, stabilize the existing
plaque and lower the risk of emboli.
• These goals are realized through a
combination of medications that are
indicated based on etiology of stroke
Blood Pressure & Antihypertensives
• 2.2 Blood Pressure Management
• The Canadian Stroke Strategy recommends
target blood pressure levels as defined by
CHEP guidelines for prevention of first
stroke, recurrent stroke and other vascular
events.
• RCTs have not defined the optimal time to
initiate blood pressure lowering therapy
after stroke/TIA. It is recommended that
blood pressure lowering treatment be
initiated (or modified) prior to discharge from
hospital. For patients with non-disabling
stroke or TIA not requiring hospitalization, it
is recommended that blood pressure
lowering treatment be initiated (or modified)
at the time of first medical assessment.
• Treatment in TIA/Previous stroke
(CHEP, 2009)
• Initial therapy:
o Treatment with combination of ACEI
& diuretic preferred
o Choice of agent will depend on
comorbidities
Other choices: ARB, Calcium
Channel Blocker, Beta
Blockers
• Second–line therapy:
o Combinations of additional agents
• Notes/Cautions:
o Recommendations do not apply to
acute stroke
o BP reduction reduces CV events in
stable patients
o Combination of an ACEI & ARB is
not recommended
Treatment
• Blood pressure reduction is generally safe
48 hours after a stroke.
• CHEP, 2009 outline 2 approaches to
management of BP in TIA/Previous Stroke
patients
• Initial therapy: ACEI in combination with a
diuretic is the preferred choice of treatment
in secondary stroke prevention. The choice
of antihypertensive will depend upon
individual comorbidities. ARBs, Ca Channel
Blockers are also choices if ACEI is
contraindicated. Studies show that 2/3 of
patients require at least 2 drugs and almost
½ of these required 3 drugs. Combination of
lifestyle and pharmacotherapy are usually
required to meet targets. Second line
therapy: If BP is not controlled with the initial
approach to treatment, CHEP suggests the
addition of medications
• Notes/Cautions: Combination of ACEI
and ARB is not recommended and
should only be considered in select
group of patients (ONTARGET):
Treatment with ACEI or ARB had similar
CV outcomes in people with CV disease
or type II diabetes
• It is important to know that the ACE Inhibitor
can cause Bradykinin release which can
cause a persistent dry cough and
angioedema (swelling of the mouth, face)
(1/500 people)
• If you experience side effects consult with
your physician immediately.
• Other side effects also include low blood
pressure, less commonly swelling of the
feet, diarrhea, headache, taste disturbance,
or feeling dizzy or faint, and possibly sexual
dysfunction
• Remember to advise the patient to have
their creatinine checked 1 week after
starting ACE Inhibitor
Patient Education: Angiotensin II Receptor
Blockers
• Well tolerated
• Contraindicated in patients with renal
stenosis
• May increase creatinine, urea and
potassium

Patient Education: Angiotensin Converting

Enzyme Inhibitor
• Take same time every day
• Contraindicated in patients with renal
stenosis
• May increase creatinine, urea and
potassium
• May have a persistent, dry cough
• Can cause angioedema (1/500)
• Other S/E:
o Dizziness, feeling faint
o Swelling of feet
o Diarrhea
o Taste disturbance
o HA
Key Points to teach your patients about ACEI
• ACE Inhibitors dilate arterial and venous
vessels by blocking the conversion of
Angiotensin I to Angiotensin II .
• In order for the medication to be effective
advise your patient to take medication at the
same time every day.