HSS 460 SCI & Stroke (Neuro pt. 2)

Anatomy & physiology of the SC

CNS tissues surrounded by articulating single vertebrae (flexible “column” designed to maximize mobility and reduce risk of injury); a structural & functional link between the brain and peripheral & autonomic nervous systems

• Carries ascending sensory input and descending motor output

• Responsible for protective reflexes

• Houses neurons sending all sympathetic output and the parasympathetic output to pelvic organs (e.g., bladder, distal colon, reproductive)

**Spinal cord injury (SCI) affects conduction of neural signals acress the site of the injury or lesion

Classification of SCI

Based on the level of the injury and the “completeness” of the injury

• Injury level refers to the lowest spinal cord segment that is uninjured (e.g., T6 means that the injury occurs at T7)

• Completeness of injury refers to the extend of neurological damage and functional loss

Tetraplegia

All four limbs and trunk have impaired function

Paraplegia

Impaired function of the trunk & legs, arms are fully functional

Complete SCI (AIS A)

No motor or sensory function is preserved below the injury (specifically, in sacral segments S4-S5 — control anal sphincter and surrounding sensation)

• Functional profiles are typically predictable

• ASIA assessment tool — assesses motor function in myotomes and dermatomes on each side of the body

Incomplete SCI (AIS B, C, or D)

Some motor or sensory function is preserved below the injury (specifically, in sacral segments S4-S5 — control anal sphincter and surrounding sensation)

• Functionality varies; numerous syndromes are associated with incomplete SCI based on preserved function

• ASIA assessment tool — assesses motor function in myotomes and dermatomes on each side of the body

Traumatic SCI

Fracture or dislocation of vertebrae surrounding spinal cord (e.g., motor vehicle accidents, falls, sports-related injuries) or direct laceration/severing of SC or nerves (e.g., gunshot or stabbing)

Nontraumatic SCI

Injury to the SC such as spinal stenosis (narrowing), congenital deformities (e.g., spina bifida), tumors, spinal stroke, or altered BP in arteries supplying the cord

Primary SC injury

Primary injury (at lesion center) occurs at the time of the initial mechanical injury and is irreversible

• Damages cell bodies, axon tracts carrying sensory/motor information, and blood vessels

Secondary SC injury

Secondary injury spreads tissue damage beyond the lesion site

• Hemorrhage, edema, acute inflammation, neurotransmitter toxicity, ion disturbanges

• Infarct of gray matter occurs in 4-8 hours if ischemia continues

• Astrocytic gliosis (“glial scarring”) occurs over the next several months

Direct (“neurological”) effects of SCI

The motor, sensory, and autonomic functional effects; “spinal shock” occurs acutely after injury, below the injury there may be…

• Flaccid paralysis and loss of deep tendon reflexes (DTRs)

• Loss of sensation

• Loss of bladder/bowel funcyion

• If tendon reflexes return within a certain time frame, neuromuscular changes may be reversible

Cardiovascular manifestations of SCI

Circulatory hypokinesis — reduced lower limb muscle contractions (skeletal muscle pump) and reduced sympathetic control of vasomotion → reduced venous return to circulation

• Decreased SV, CO, and BP

• Venous stasis, deep thrombosis (DVT), and pulmonary embolus may occur

• Increased risk of orthostatic hypotension (OH) and exercise-induced hypotension (EH)

• Depending on injury level, sympathetic control over HR may be absent or diminished

Pulmonary manifestations of SCI

• Ventilation impairment, especially in individuals with tetraplegia

• Reduced function of diaphragm (C3, 4, 5 keep the diaphragm alive), intercostal, and abdominal muscles

Bowel and bladder manifestations of SCI

Neurogenic bowel and bladder dysfunction → loss of voluntary voiding of either/both may necessitate self-catheterization and manual voiding of bowel

Musculoskeletal manifestations of SCI

• Marked muscular atrophy

• Increased risk of pressure ulcers due to exposure of bony prominences

• Increased risk of neurogenic osteoporosis

Endocrine manifestations of SCI

Impaired glucose tolerated and hyperinsulinemia due to muscle atrophy, increased adiposity, and adrenal gland dysfunction

Autonomic dysreflexia

Associated with injuries at T6 and above, where sympathetic output to viscera and related vessels is no longer regulated by higher brain centers

• Noxious sensory stimulus → exaggerated sympathetic response below injury level → acute vasoconstriction & hypertension

• Baroreceptor activation → vagal-induced bradycardia & acute vasodilation above injury level

• Strong cutaneous or visceral stimuli can include: pressure ulcers & dressing changes, overly stretched bladder/bowel, bladder infection, ingrown toenails, cuts, bruises, even ejaculation

Warning signs of autonomic dysreflexia

• Above injury level: vasodilation, slowed HR, sweating, flushed skin, headache

• Below injury level: vasoconstriction, increased BP, pale/cool/clammy skin, goose bumps (piloerection)

Stroke

Aka cerebrovascular accident (CVA) or “brain attack”; a syndrome of neurological deficits resulting from loss of blood flow to a region of the brain

Ischemic stroke

Obstruction of cerebral blood vessel(s) by thrombus or embolus; usually due to atherosclerosis in cerebral circulation or cardiogenic embolus

• 87% of all strokes

• The atherosclerotic process that causes cerebrovascular disease and ultimately an ischemic stroke, proceeds in the same fashion as plaque progression in CAD and PAD

• The traditional and nontraditional risk factors of CAD and PAD are associated with development of ischemic cerebrovascular disease

Thrombotic ischemic stroke

Arterial occlusion (obstruction) occurs as a clot forms on atherosclerotic plaque

Embolic ischemic stroke

A piece of thrombus becomes mobile in the blood and “wedges” in the downstream artery that matches its size

• This is most often the middle cerebral artery (MCA) when the thrombus source is the internal carotid artery

Ischemic penumbra

The “halo” of ischemic tissue surrounding the central area of infarction (necrosis)

• Like the area of ischemia surrounding the area of necrosis in ACS

Transient ischemic attack (TIA)

A warning of impending ischemic stroke (“mini-stroke”); represents ischemia that reverses before there is infarct

• Like angina that serves as a warning associated with ACS

Hemorrhagic stroke

Excessive bleeding into neural tissue

• Hypertension is a major risk factor

• Also associated with age & fragility of blood vessels, aneurysm, and arteriovenous (AV) malformations

Cerebral aneurysms

Cerebral aneurysms = “berry” aneurysms

• Most common in Circle of Willis

• Mortality rate associated with rupture is 33-50%

• Symptoms include:

  • Atypical headaches for days to weeks prior to rupture; nausea and vomiting may accompany

  • Sudden, severe headache at rupture

  • Can occur at any time; most often with increased ICP (e.g., coughing, bowel movement)

Hemorrhagic strokes due to arteriovenous (AV) malformations

Etiology — congenital lack of connecting capillaries between arteries and veins → results in “tangles” of AV malformations

• Blood in high pressure arteries flows directly into thin-walled veins

• Symptoms include severe, throbbing headaches

• Once discovered, the AV malformation can be surgically removed or artificially blocked to prevent blood flow

Stroke symptoms

• Numbness, weakness, and/or paralysis of the face, arm, or leg

  • This will be contralateral because of cerebral control of voluntary motor and somatic sensory information

• Confusion, speech problems (e.g., slurring), and cognitive defects

• Impaired bilateral or unilateral vision

• Impaired coordination and walking

• Headache

• Memory loss