Neurological: Stroke, TBI and SCI

Question 1

Right CVA characteristics

Answer 1

o Distorted awareness and impression of self
o Denial of disability, rigidity of thought, short attention span
o decreased musical and artistic awareness, spatial and pattern perception, recognition of faces, emotional content of language (speak in monotonous voice), discriminating smells, damage to right brodmann’s area have difficulty differentiating smells
o Use Verbal Cues

Question 2

Left CVA characteristics

Answer 2

o Diminished functional speech, aphasias
o Most muscles on R side of body are affected. Also decr, numerical and scientific skills, spoken and written language, sign language.
o Tx: maximum use of demonstration and gesture to assist in re-learning motor tasks

Question 3

Treatment strategies for neglect

Answer 3

If neglect: incorporate involved side into crossing midline activities (rolling, using PNF lift pattern)

Question 4

PIVOT transfer to affected side has the following benefits:

Answer 4

o Retrains motor control through weight shift and WB on affected side
o Decreases extensor strategy by WB and maintaining minimal knee flexion
o Directs attention and vision to affected side

Question 5

What is a strategy to decrease FLEXOR TONE in the upper limb

Answer 5

WBing and rocking on extended UE

Question 6

How would you position a patient if they were presenting with acute and flaccid UE..

Answer 6

o Position in side-lying on good side with affected shoulder in protraction and arm extended resting on a pillow (avoid flexion-adduction of UE as spasticity typically develops)

In supine, pillow under elbow with forearm in extension and hand supported on pillow

Question 7

What is a good exercise if a patient was demonstrating strong hemiplegic synergies..

Answer 7

Use BRIDGING W/ pelvic elevation (combines hip extension from the extensor synergy and knee flexion from the flexor synergy

Question 8

Cerebral arteries and effects if occlusion:

- Internal carotid

Answer 8

Collateral supply is possible thru ant. and middle cerebral arteries; deficit=contralat. hemiplegia and hemisensory disturbance, global aphasia (if dominant side), mentally slow, contralateral homonymous hemianopia, partial Horner’s syndrome, gaze palsy (eyes to opp side); is the main supply for ant cerebral a., post CA, middle cerebral a.
o Supplied CNS (whereas external carotid artery supplies face and parts of neck

Question 9

Cerebral arteries and effects if occlusion:

Anterior cerebral artery:

Answer 9

Weakness and sensory loss of contralat limbs, self care problems, emotional lability, mild apraxia
o LE more affected than UL

Question 10

Cerebral arteries and effects if occlusion:

Middle cerebral artery

Answer 10

Most commonly occluded in a left hemisphere stroke.
o Presentation: contralat hemiplegia, hemisensory loss, hemianopia, contralat neglect, aphasia (impaired language ability); if on dominant side: apraxia; impaired hearing, difficulty dressing; may also produce motor speech dysfunction (Broca’s area); eyes may deviate to NON-affected side
o Can have UE more affected theb LE

Question 11

Cerebral arteries and effects if occlusion:

Posterior cerebral artery (PCA)

Answer 11

Supplies occipital lobes; vision problems, CN III palsy, contralateral hemiplegia, chorea (abnormal invol. mvmts, looks like dancing), hemiballismas (involuntary flinging mvmts of extremities), hemisensory impairment, contralat homonymous hemianopia, difficulty with naming and colors, dyslexia, difficulty naming people in sight
o involves the main trunk, sensory aphasia (dominant side), loss of superficial touch, and deep sensation.

Question 12

Cerebral arteries and effects if occlusion:

Vertebral artery

Answer 12

Two join to form basilar artery; imp branches to watch for strokes PICA (largest branch of vertebral a.), AICA, PCA
o Presentation: areflexia, coma, confusion, dizziness, and headache

Question 13

Cerebral arteries and effects if occlusion:

Vertebrobasilar artery involvement

Answer 13

Loss of consciousness, may be comatose/vegetative state; no ability to speak; may have either hemiplegia or quadriplegia

Question 14

Cerebral arteries and effects if occlusion:

Superior cerebellar artery

Answer 14

Supplies cerebellum, limb ataxia, Horner’s syndrome (droopy eyelid, red face), contralateral sensory loss

Question 15

Cerebral arteries and effects if occlusion:

Anterior inferior cerebellar (AICA)

Answer 15

Supplies cerebellum, ipsilateral limp ataxia, ipsilateral horner’s, sensory loss, facial weakness, paralysis of lateral gaze, and contralateral sensory loss of limbs and trunk

Question 16

Cerebral arteries and effects if occlusion:

Posterior Inferior Cerebellar Artery (PICA)

Answer 16

supplies cerebellum;
Will see: dysphagia, ipsilateral limb ataxia, vertigo, nystagmus, nausea, ipsilateral horners, sensory loss (p and temp) of face, pharyngeal and laryngeal paralysis, contralateral sensory loss (p and temp) of trunk, visual sy’s (paralysis of vertical eye mvmts and decrd pupillary light reflex)
o Presents with “Lateral Medullary (Wallenberg’s syndrome)

Question 17

Broca’s (Expressive or nonfluent) aphasia

Answer 17

Broca’s area is located in the left frontal lobe and is responsible for expressive speech; can understand verbal cues, but impaired motor production of speech
o Use verbal cues in communication

Question 18

Wernicke’s (Receptive or fluent) aphasia=

Answer 18

Wernicke’s area is located in the left temporal lobe and is responsible for receptive speech; spontaeouns speech is preserved and auditory comprehension is impaired
o Use demonstration and gesture (visual modalities) for communicating

Question 19

Define diffuse axonal injury (DAI)

Answer 19

Deceleration and shearing of the brain’s long connecting nerve fibers
o Usually causes a coma, can’t see on MRI; can affect grey/white matter interfaces

Question 20

Differentiate between primary and secondary brain injury

Answer 20

Primary brain injury: damage caused at time of impact

Secondary brain injuries = cerebral blood flow is 50% less than normal post injury, bruising, inflammation,

Question 21

What is the treatment and general management of acute TBI?

Answer 21

• Intracranial pressure: normal is 0-10 (or 10-15) mm Hg; >20mm Hg is BAD = brain damage –> HOB 30’
• head down positioning is CONTRAINDICATED! ***
• Positioning: limit neck flex and rotation
• Suctioning: pre/post oxygenation at 100% O2
• Resting splints 6-8hrs to prevent contractures
• Aspiration risks: turn feed tube off 20mins prior to Tx

Question 22

What are the features of an intracranial epidural bleed

Answer 22

o Rapid bleeding between cranial vault and dura; 90% assocd with skull fractures, most often in temporal or temproparietal region; arterial bleed (ex middle meningeal artery)
 Classic presentation: “Talk and die” – initially pt feels normal, then decline in mental status assoc with decline in neuro exam until LOC
 Tx: medical emergency, ensure ABC’s, transport immediately

Question 23

What are the features of an intracranial sub-dural bleed

Answer 23

Blood collects between brain and dura, often requires surgical intervention (burr holes or craniotomy), low pressure venous bleed
 S&S: fluctuating symptoms, seem drunk

Question 24

What are the features of an intracranial subarachnoid bleed

Answer 24

Very high pressure; occasional CN 3 (occulomotor) warning signs; arterial bleed (often in areas of Circle of Willis)

Question 25

Differentiate between decerebrate and decorticate posturing

Answer 25

Decerebrate posturing= damage below red nucleus; indicates brain stem damage (lesions or compression in midbrain) and lesions in cerebellum (injury to the diencephalon, pons, or midbrain.)
o Rigid extension of all limbs
o lower extremities plantar flexed and fully extended, forearm pronated, and wrist flexed.

Decorticate posturing= lower extremities plantar flexed and internally rotated and the upper extremities positioned in shoulder adduction, elbow flexion, and wrist flexion
 UE Flexion and LE extension
 damage above red nucleus; areas including cerebral hemisphere, thalamus, cord, corticospinal tract

Question 26

Define;

• Hyperpathia
• Deep Anal Pressure (DAP)
• Voluntary Anal Contraction
• Complete injury
• Zone of Partial Preservation

Answer 26

• Hyperpathia=everything feels sharp
• Deep Anal Pressure (DAP): if present, Pt has a sensory incomplete injury ASIA B or higher
• Voluntary Anal Contraction=if present indicates motor incomplete (AISA C or higher)
• Complete injury = no sensory or motor Fx is preserved in the sacral segments S4-S5; there may be dermatomes below the sensory level and myotomes below the motor level that remain partially innervated
• Zone of Partial Preservation, the most caudal segment with some sensory defines extent of ZPP

Question 27

Characteristics of Central Cord syndrome

Answer 27

• Most common syndrome seen and can be very disabling
• Damage to the central portion of the cord and an incomplete lesion
  caused by hyperextension injury of neck, usually an elderly person who falls
• Presents with greater loss of UE function compared to LE (will lose most ADL function, have no mechanism to save self when falling)
• Often associated with spinal canal stenosis

Question 28

Characteristics of Brown Sequard Syndrome

Answer 28

• Traumatic neurological disorder resulting from compression of one side of the spinal cord or hemisection, typically seen after a penetrating/knife-type injury; asymmetrical damage to cord
• IPSILATERAL loss of proprioception/vibration sense and motor control at/below level of lesion
• CONTRALATERAL loss of pain and temperature sensation a few levels below the lesion
• Sensory loss at level of lesion

Question 29

Characteristics of Anterior Cord Syndrome

Answer 29

• Relatively rare, but can happen from occlusion of blood supply to anterior cord
• Bilateral Loss of motor function, pain and temperature (anterior tracts) below injury level
• Preservation of light touch and proprioception (posterior tracts) - dorsal columns spared
• Sparing of proprioception is NOT a good indicator of better prognosis

Question 30

Characteristics of Cauda Equina Syndrome

Answer 30

• Spinal cord terminates at L1-L2; injuries at conus can affect both conus and root resulting in a varied neuro picture; i.e. mixture of UM and LMNL
• Damage to lumbar and sacral nerve roots (L2 & below)
• Lower motor neuron type injury
• Variable loss, areflexic (flaccid) bowel and bladder
• Affects more than one nerve root, surgical emergency
• Usually presents with: bilateral leg pain/numbness, sacral root problems, urinary retention, stool incontinence, absent reflexes

Question 31

Characteristics of Conus Medullaris Syndrome

Answer 31

• Very similar to cauda equina syndrome, but with some UMN injury features
• May be sparing of sacral reflexes

Question 32

What is a good prognostic indicator for neuro injuries

Answer 32

Pinprick preservation (LE and sacral) w/in 72hrs is good prognostic indicator of motor function to return and ability to walk

Question 33

Exs recommendations post SCI

Answer 33

F - Minimum = 2 days/week,
I - RPE 11-14; BORG (HR and BP will not be normal d/t lack of sympathetic response)
T - 30-40 min, 3x/week for greater than 12 weeks to see increase in aerobic capacity
T - Strength train 2-3 times/week (cautious of orthopedic injury, esp wrist and shoulder tendinopathy)

Question 34

SCI effects on respiratory function;

• Cough
• Respiratory muscles

Answer 34

o C1-C3 absent, C4-T1 non functional, T2-T4 poor, T5-T10 weak, T11 and below is normal

o C4 is normally the level Pt’s need to breathe independently
o C2-C7 innervate accessory mm of breathing
o T11 and below, normal vital capacity
o T1-T11 intercostals
o T6-L1 abdominals

Question 35

Autonomic effecrs of SCI on the nervous system

• Sympathetic nervous system
• Parasympathetic nervous system
• With injuries above or equal to T6

Answer 35

 Sympathetic NS- Chain T1-L1, fight or flight, increases HR and BP and blood flow to skeletal mm, RELAXES bronchial mm (one would think it would contract them BUT if a bear was chasing you, you would want the mm to relax to incr O2 supply)

 Parasympathetic NS- Cranial nerves 3, 7, 9, 10 and S2-4; primary interest in Vagus nerve; decreases HR and contractility, decr blood flow to smooth mm, contracts bronchial mm

 With Level of injury T6 and above: (in general)
o Sympathetic influence is dependent on level of injury (b/c it goes from T1-L1)
o Parasymp influence remains intact and UNOPPOSED via the vagus nerve in injuries T6 and higher
o Limits cardiac output and shunting of blood from inactive to active ones
o Blunting of heart rate often to only 110-120bpm
o Heart response is d/t vagal withdrawal rather than sympathetic drive

Question 36

What is the difference between spinal shock and neurogenic shock
- What are the 3 clinical signs of neurogenic shock?

Answer 36

 Spinal Shock = temporary suppression of all reflex activity below the level of injury (24-48 hrs)
o Depending on the extent of the lesion, the pt may lose all or some of their sensation & motor activity below the level of the lesion

 Neurogenic shock (T6 and above)= body’s response to sudden loss of symp. control, therefore parasymp dominance, loss of vasomotor control;
o 3 clinical signs are 1) bradycardia, 2) hypotension, 3) Hypothermia
o Rx for hypotension: volume resuscitation (saline), vasopressors (to counter loss of sympathetic tone)

Question 37

What is post traumatic syringomyelia?

- what are the signs and symptoms

Answer 37

 Post traumatic syringomyelia = a formation of an abnormal tubular cavity (cyst) in the spinal cord; the dura tethers/scars to the arachnoid blocking CSF flow, CSF is forced into the spinal cord progressively enlarging the cyst which compresses the cord and its vascular supply; cyst develops below level of lesion
o S&S: LMN symptoms, spasms, phantom sensation, reflex changes, autonomic changes

Question 38

Differentiate between spastic and flaccid bladder

Answer 38

 Spastic bladder = injuries above the conus, messages will continue to travel b/w bladder and spinal cord since reflex arc is still intact, may be triggered by “tapping”, bladder can be trained to empty on its own, bladder mngmt is either intermittent catheters or condom/foley drainage
 Flaccid bladder= in conus and cauda equina injuries, messages don’t travel b/w spinal cord and bladder since the reflex centre is damaged, bladder loses ability to empty reflexively, bladder will continue to fill AND must be catheterized
 Reasons for dizziness in SCI pt: autonomic dysreflexia, orthostatic hypotension, hypoglycemia