Neurological Alterations

What are the 2 causes of stroke?

• Ischemia → inadequate blood flow to part of the brain

• Hemorrhage → bleeding into the brain

• Result = death of brain cells

Other terms for stroke

• Brain attack (emphasizes urgency)

• CVA

Impact of strokes

• Loss or impairment of functions controlled by affected brain area

  • Movement, sensation, thinking, talking, emotions

Common disabilities from strokes:

• One-sided weakness

• Inability to walk

• Dependence for their ADLs

• Aphasia (can’t communicate)

• Depression

Leading cause of serious long-term disability =

Strokes

BE FAST (stroke S&S)

B – Balance; sudden loss of balance or coordination, headache, dizziness

E – Eyes; sudden vision changes or loss of vision in one or both eyes

F – Facial drooping (uneven smile/face?)

A – Arm weakness (one arm drifts down; pronator drift?)

S – Speech difficulties (slurred, unable to repeat sentence)

T – Time to call 911 (note time symptoms started!)

BE FAST (stroke S&S)

• Balance; sudden loss of balance or coordination, headache, dizziness

• Eyes; sudden vision changes or loss of vision in one or both eyes

• Facial drooping (uneven smile/face?)

• Arm weakness (one arm drifts down; pronator drift?)

• Speech difficulties (slurred, unable to repeat sentence)

• Time to call 911 (note time symptoms started!)

Brain’s blood supply =

• Brain is very metabolically active, requiring 750-1000 mL/min (20% of CO)

  • No capacity of O2 or glucose

• Supplied by internal cartoid arteries (anterior) and vertebral arteries (posterior)

• Connected by circle of Willis

Critical timeline for strokes/TIAs

• 30 seconds = neuroloigc metabolism altered

• 2 minutes = metabolism stops

• 5 minutes = cell death occurs

How does the brain protect itself?

Autoregulation:

• Maintains constant blood flow despite BP changes (50-150 mm Hg)

  • Adjusts vessel diameter

• May be be impaired after stroke (protective mechanism can be comprimised by stroke/TIA)

  • Brain is then dependent on systemic blood pressure

• CO2 levels strongly affect cerebral blood flow

• After stroke, there may be angiogenesis/collateral cirucatlion over time to increase perfusion

Why do we not lower the BP too rapidly or too much after a patient has had an acute stroke?

• Brain’s ability to autoregulate (protective mechanism which adjusts vessel diameter) is damaged

• Brain is now dependent on systemic BP for adequate perfusion; brain may need higher pressures to maintain function w/o autoregulation

How does CO2 affect cerebral blood flow?

CO2 is a potent vasodilator; we monitor respiratory status of stroke patients since we don’t want these patients to hyperventilate; if they have low CO2, they start having vasoconstriction which can reduce blood flow to brain

What is autoregulation?

• Protective mechanism that maintains constant blood flow to brain despite BP changes (50-150 mm Hg, as in cardiac arrest)

  • Adjusts vessel diameter

• May be be impaired after stroke (protective mechanism can be comprimised by stroke/TIA)

  • Brain is then dependent on systemic blood pressure

Why can hyperventilation be dangerous for stroke patient?

CO2 is a potent vasodilator; if CO2 levels, there will be vasoconstriction, which lowers perfusion to the brain.

Significance of angiogenesis/collateral circulation in stroke patients

Some stroke patients (e.g. ones that have vessel stenosis) will have more collateral circulation/agiogenesis that occurs over time that improve lateral blood flow, so when they have a full-blown stroke, they don’t have as many symptoms as somebody who suddenly gets a stroke from an embolislm.

Nonmodifiable risk factors for strokes

• Age (risks double each decade after 55)

• Gender (more common in men, but women die more often)

• Race/ethnicity (Blacks 2x higher risk)

• Family hx/genetics

Major modifiable risk factors for strokes (modifiable risk factors cause 90% of strokes)

• HTN (single most important risk factor)

• Heart disease (especially Afib → 25% of strokes)

  • Afib patients need to be on anticoagulation therapy

• Obesity (metabolic syndrome)

• Physical inactivity

• Poor diet

• Diabetes (5x higher risk)

• Alcohol/drug use

• Smoking (2x ischemic stroke risk, and 4x hemorrhagic stroke risk)

  • risk normalizes after 5-10 years if they quit; still important for patient who smoked for 30 years as they can normalize it.

What is the sing;e most important modifiable risk factor for strokes?

HTN

HHOPPDAS Major modifiable risk factors for strokes

H – HTN

H – Heart disease (Afib = 25% of strokes

O – Obesity

P – Poor diet

P – Physical inactivity

D – Diabetes

A – Alcohol/drug use

S – Smoking (2x ischemic, 4x hemorrahgic)

• Transient neurologic dysfunction from focal brain/spinal cord/retinal ischemia

• Has NO acute infarction (no permanent brain damage)

• Symptoms typically last <t hour

• Medical emergency → treat immediately

TIA

Outcomes for TIAs

• 1/3 have no further events

• 1/3 have more TIAs

• 1/3 progress to stroke

ABCD² Score (0-7 points)

• Predicts r/o stroke after TIA

  • A – Age ≥ 60 years (1 point)

  • B – BP ≥ 140/90 (1 point)

  • C – Clinical features (1-2 points)

  • D – Duration ≥ 60 min (2 points) or 10-59 min (1 point)

  • D – Diabetes (1 point)

Why is TIA a medical emergency and needs immediate treatment?

• TIAs are a major indication of cerebrovascular disease; these patients have a high risk of having a stroke later

• Furthermore; there is no way for patient to differentiate between a stroke and TIA for sure unless they are evaluated

• TREAT IT LIKE A STROKE

Common symptoms of TIAs (similar to strokes)

• Amaurosis Fugax/vision loss in one eye (temporary and painless loss of vision in one or both eyes due to disruption of the blood flow to the retina; feel like current dropping over your vision)

• Unilateral weakness or numbness

• Sudden speech difficulty

• Dizziness/loss of balance

Significance of ABCD²

• 0-3 = 1% 2-day stroke risk

• 4-5 = 4.1% risk

• 6-7 = 8.1% risk

• Higher scores may need hospitalization and aggressive management to identify and address any underlying causes

Imporant education regarding TIAs for patients

• Treat it like a stroke (subsequent episodes need to be treated as a stroke since they have same symptoms even if they had a TIA before)

• TIA = risk for stroke

• Aggressive monitoring/care is necessary

“Clogged pipe.” Stroke (87%) that results from inadequate blood flow from a partial or complete arterial occlusion. has two types:

• Thrombotic (most common ~60%)

• Embolic

Ischemic stroke

“Bursted pipe.” Stroke (13%) that results from bleeding into brain tissue. Has two types:

• Intracerebral hemorrhage

• Subarachnoid hemorrhage (SAH)

Hemorrhagic stroke

TIA vs stroke

• TIA = ichemia w/o infarction

• Stroke = infarction (cell death)

Stroke diagnosis

• #1 imaging is CT and is fast/convenient (can quickly rule out hemorrhage)

  • If not hemorrhage on CT but has significant stroke sx, it’s probably ischemic stroke → give tPA

• MRI is better, but is slower than CT

• Blood clot forms in brain artery

• Clot develops at site of atherosclerotic plaque

• Most common stroke type (~60%)

• More common in older adults

These are characteristics of what condition?

Thrombotic strokes

Risk factors for ischemic strokes (thrombotic)

• HTN

• DM

• High colesterol

• Atherosclerosis

Clinical presentation of thrombotic strokes

• Often occurs during or after sleep

• TIA may precede (30-50% of cases)

• Stepwise progression of symptoms

• Usually conscious in first 24 hrs

• Symptoms may progress over 72 hrs as edema increases

• Symptoms are not very severe, but worsen with time (or they can wake up fucked).

• Often occurs during or after sleep (may be due to decreased BP during sleep)

• TIA may precede this (30-50% of cases)

• Stepwise progression of symptoms (sx worsen in stages)

• Usually conscious in first 24 hrs

• Symptoms may progress over 72 hrs as edema/swelling increases

• Symptoms are not very severe, but worsen with time (or they can wake up fucked).

These are clinical manifestations of what condition?

Thrombotic strokes

Strokes that often have TIAs preceding them

Thrombotic strokes

• Traveling clot lodges in cerebral artery

• Second most common cause of ischemic strokes

• Has sudden onset with severe sx (acute)

These are characteristics of what condition?

Embolic strokes

Common sources of embolic strokes

• Heart conditions: Afib (most common), MI, endocarditis, valve problems

• Atherosclerotic plaque breaking off; any clot that breaks off e.g. DVT

• Less common: air embolism, fat from long bone fractures

Clinical presentation of embolic strokes

• Usually occurs during activity

• Sudden, severe neurologic deficits (no warning signs!)

• Often no warning signs

• Patinet usually conscious, may have HA

• Symptoms may be temporary if clots breaks up

• High recurrence rate w/o tx

• Usually occurs during activity

• Sudden, severe neurologic deficits (no warning signs!)

• Often no warning signs

• Patinet usually conscious, may have HA

• Symptoms may be temporary if clots breaks up

• High recurrence rate w/o tx

These are clinical manifestations of what condition?

Embolic strokes

Why is cardiac workup essential for all stroke patients?

• Flag HTN and atherosclerosis

• Flag heart conditions that increase risk for embolic strokes e.g. Afib

• Bleeding within brain tissue (usually basal ganglia); increased ICP

• Most lethal type of stroke

  • 30-day mortality: 40-80%

  • Half of deaths occur in first 48 hrs

• Most common cause = HTN

These are characteristics of what condition?

ICH

Most common cause of ICH

Chronic uncontrolled HTN

• Over time, HTN damages small blood vessels over time, making them more prone to ruptue → bad things happen

Causes of ICH

• HTN

• Vascular malformations

• Anticoagulant/thrombolytic drugs

• Coagulation disorders

• Trauma, tumors, ruptured aneurysms

• Occurs during activity (BP spikes)

• Sudden onset with rapid progression (minutes to hrs)

• Severe HA, nausea, vomiting

• Decreased LOC

• HTN

These are clinical manifestations of what condition?

ICH

Patient with head trauma and is on anticoagulant therapy →

Must be screened for ICH; these patients are at higher risk, especially elderly patients

Clinical presentation of ICH

• Occurs during activity (BP spikes)

• Sudden onset with rapid progression (minutes to hrs)

• Severe HA, nausea, vomiting

• Decreased LOC (may be unconscious due to ICP)

• Deficits are dependent on location/size

• HTN

LOC comparison between ischemic stroke or hemorrhagic stroke

• Ischemic strokes may have patients who remain conscious.

• Hemorrhagic stroke patients often come in unconscious

Cerebellar hemorrrhages (ICH) symptoms =

More severe HA, vomiting, inability to walk, eye movement.

Putaminal hemorrhage (ICH) symptoms =

• More common

• Unilateral weakness, slurred speech, eye deviation

Thalamic bleeds (ICH) symptoms

• Sensory loss

• Motor loss

Pontine hemorrhgaes (ICH) symptoms

• Most serious since this affects basic life functions

• These patients may go into a coma

• Complete paralysis and abnormal VS

Treatment for hemorrhagic strokes

• Controlling BP

• Managing ICP

• Cerebrovascular and cardiac function monitoring and maintenance

• Surgery to evacuate hematomas

• NO BLOOD THINNERS

• Bleeding into CSF-filled space between arachnoid and pia mater

• Often caused by ruptured cerebal aneurysm

These are characteristics of what condition?

SAH

Aneurysm types (SAH)

• Saccular (berry) aneurysms → 2-30 mm

• Fusiform atherosclerotic aneurysms

• Most located in circle of Willis

Stroke often caused by ruptured cerebral aneurysm

SAH

Clinical presentation of SAH

• “Worst HA of my life,” thunder clap HA

• Sudden onset during activity (NO WARNING SIGNS until vessel explodes)

• NV, seizures

• Stiff neck

• Loss of consciousness (may or may not occur)

• Focal neurologic deficits (blood mixes with CSF, causing irritation and increased ICP)

• Neurosurgical emergency

• “Worst HA of my life,” thunder clap HA

• Sudden onset during activity (NO WARNING SIGNS until vessel explodes)

• NV, seizures

• Stiff neck

• Loss of consciousness (may or may not occur)

• Focal neurologic deficits

• Neurosurgical emergency

These are clinical manifestations of what condition?

SAH

Risk factors for SAH

• HTN

• Smoking

• Cocaine/stimulants

• Family hx

• If 2 or more first-degree relatives → need screening

Anything that increases BP (e.g. activity or stimulant drugs) =

Increased r/o hemorrhagic strokes

Major complications of SAH

• Rebleeding before tx

• Cerebral vasospasm (peaks 6-10 days post-bleed)

What is the significance of cerebral vasospasms in SAH?

• Causes an ischemic stroke on top of the hemorrhage

• Body’s compensatory mechanism to protect brain, by constricting blood vessels to slow bleeding; this backfires

• Risk peaks at 6-10 days after initial bleed; SAH patients need ICU monitoring for up to 2 weeks (risk for vasospasm after origianl injury)

Tx of SAH caused by aneurysm

• Surgery (clipping/coiling)

• Manage vasospasms with meds → maintain adequate BP and fluid volume

• Watch for rebleeding

Right brain damage (stroke) =

• Left-sided deficits

• Left-sided hemiplegia/hemiparesis

• Spatial-perceptual deficits (trouble judging distances, navigating spaces)

• Quick, impulsive bahvior

• Poor judgment

• Neglect of left side

• HIGH FALL RISK

Left brain damage (stroke) =

• Right-sided deficits

• Right-sided hemiplegia/hemiparesis

• Aphasia (speech/language problems)

• Slow, cautious behavior

• Awareness of deficits → anxiety, depression

Stroke on right side of brain =

• Paralyzed left side: hemiplegia

• Left-sided neglect

• Spatial-perceptual deficits

• Tends to deny or minimize problems

• Rapid performance, short attention spain

• Impulsive → safety problems

• Imparied judgment

• Impaired time concepts

Stroke on left side of brain =

• Paralyzed right side: hemiplegia

• Imparied speech/language aphasia

• Impaired right/left discrimination

• Slow perforamnce, cautious

• Aware of deficits → depression/anxity

• Impaired comnprehension related to language, math

Artery-specific manifestations of strokes

• Anterior cerebral → leg > arm weakness, personality changes

• Middle cerebral → arm > leg weakness, aphasia (dominant side), neglect (non-dominant)

• Posterior cerebral → visual deficits, hallucinations

• Vertebrobasilar → cranial nerve deficits, vertigo, ataxia, coma risk

Effect of stroke on ACA (sx)

Leg > arm weakness, personality changes

Effect of stroke on MCA (sx)

• Classic stroke sx

  • Arm > leg weakness

  • Hemiparesis

  • One-sided sensory loss

  • Aphasia (dominant side)

  • Neglect (non-dominant)

Effect of stroke on PCA (sx)

• Visual deficits

• Hallucinations

• Balance/coordination

• Decreased LOC if brainstem is involved

Effect of stroke on vertebrobasilar artery (sx)

Cranial nerve deficits, vertigo, ataxia, coma risk

MCA stroke has what symptoms?

• Classic stroke sx

  • Arm > leg weakness

  • Hemiparesis

  • One-sided sensory loss

  • Aphasia (dominant side)

  • Neglect (non-dominant)

Vertebrobasilar artery stroke has what symptoms?

Cranial nerve deficits, vertigo, ataxia, coma risk

ACA stroke has what symptoms?

Leg > arm weakness, personality changes

PCA stroke has what symptoms?

• Visual deficits

• Hallucinations

• Balance/coordination

• Decreased LOC if brainstem is involved

Motor deficits from stroke result from:

Destruction of motor neurons in pyramidal pathway

Pattern of recovery of motor function after stroke

• Initial → flaccidity, hyporeflexia (days to weeks)

  • If flaccid for too long = bad, we want spasticity (spasticity means nervous system is reconnecting itself)

• Progression -. spasticity, hyperreflexia develops

• Gradual return of voluntary movement (proximal and gradually to distal)

Characteristics of motor deficits from stroke

• Contralateral deficits (opposite side from brain lesion)

• Weaknes sor paralysis (hemiparesis/hemiplegia)

• Loss of skilled voluntary movement (akinesia)

• Altered muscle tone

• Changed reflexes

• MCA stroke: upper extremity > lower extremity weakness

Position tendencies (motor deficits of strokes) nursing implications

• Need to position patient’s joints correctly to avoid injury and pain

  • When they’re flaccid, day oen we want to position joints correctly so they don’t get injury from flaccidity

• Shoulder → internal rotation

• Arm → flexion contractures at hand, wrist, elbow

• Hip → external rotation

• Foot → plantar flexion (footdrop)

Nursing interventions for contractures (motor deficits after stroke)

When patient is flaccid; day one we want to position joints correctly to avoid pain and injury as patient gradually becomes more spastic → maintain alignment of joint

• Trochanter rolls

• Arm supports

• Hand cones

• Leg splints

• High top shoes

Communication deficits of strokes

• Broca’s aphasia

• Wernicke’s aphasia

• Global aphasia

• Dysarthria

• Frontal lobe damage

• Understand speech BUT can’t speak fluently

  • Broc → broken speech

• Short, effortful phrases, omits small words

• Aware of problem → frustration

• Example: “Walk dog” for “I will take the dog for a walk)

These are clinical manifestations of what condition?

Broca’s aphasia (nonfluent/expressive)

• Temporal lobe damage

• Speaks fluently BUT doesn’t make sense

  • Wer = word salad

• Can’t understand speech

• Unaware of errors

• Example: “You know that smoodle pinkered…”

These are clinical manifestations of what condition?

Wernicke’s aphasia (fluent/receptive)

Describe Broca’s aphasia (nonfluent/expressive)

• Frontal lobe damage

• Understand speech BUT can’t speak fluently

  • Broc → broken speech

• Short, effortful phrases, omits small words

• Aware of problem → frustration

• Example: “Walk dog” for “I will take the dog for a walk)

Describe Wernicke’s aphasia (fluent/receptive)

• Temporal lobe damage

• Speaks fluently BUT doesn’t make sense

  • Wer = word salad

• Can’t understand speech

• Unaware of errors

• Example: “You know that smoodle pinkered…”

• Extensive language area damage

• Severe communication difficulties

• Limited speaking AND understanding

These are clinical manifestations of what condition?

Global aphasia

• Muscular control problem

• Slurred speech, poor articulation

• Language and comprehension intact

These are clinical manifestations of what condition?

Dysarthria

Describe global aphasia

• Extensive language area damage

• Severe communication difficulties

• Limited speaking AND understanding

Describe dysarthria

• Muscular control problem

• Slurred speech, poor articulation

• Language and comprehension intact

What type of strokes cause aphasia?

Left-sided strokes

Communication strategies for patients with aphasia

• Simple sentences

• Be patient; allow ample time to respond

• Use gestures or pictures

• Maintain calm environment

• Goal is to teach patients how to communicate their own needs rather than speak for them

  • Consult speech therapy

Emotional/affect changes of strokes

Joker syndrome

• Emotional lability (unpredictable mood swings)

• Pseudobulbar affect (inappropriate crying/laughing)

• Depression/anxiety

• Apathy

Other stroke manifestations

• Emotional/affect changes

  • Joker syndrome + apathy (labile, depressed, inappropriate laughing/crying unrelated to actual feelings) → loss of emotional control mechanisms regulated by brain

    • Teach patient it’s a neurological sx, NOT a psychological sx

• Spatial-perceptual problems

  • e.g. homonymous hemianopsia

• Neglect syndrome (ignores affected side; may have blindness in one side or do not notice things on affected side)

  • Position food on unaffected half of plate

• Agnosia (can’t recognize objects e.g. may not recognize fork even when looking at it)

• Apraxia (can’t perform learned sequential movements e.g. not able to brush teeth)

• Elimination

  • Urinary urgency, frequency, incontinence (usually temporary)

  • Constipation (immobility, weak abd muscles)

• Intellectual function

  • Memory impairment, impaired judgment, difficulty w/ abstract thinking

Stroke patient ignores affected side; may have blindness in one side or do not notice things on affected side

• Position food/ on unaffected half of plate

This is called =

Neglect syndrome

Stroke patient can’t recognize objects e.g. may not recognize fork even when looking at it. This is called =

Agnosia

Stroke patient' can’t perform learned sequential movements e.g. not able to brush teeth. This is called =

Apraxia

What problems with elimination do stroke patients have?

• Urinary urgency, frequency, incontinence (usually temporary)

• Constipation (immobility, weak abd muscles)

What problems with intellectual function do stroke patients have?

Memory impairment, impaired judgment, difficulty w/ abstract thinking

Spatial-perceptual alteration wher epatient doesn’t recognize a whole side of what’s going on in their body.

Homonymous hemianopsia

Diagnostic studies for stroke

• Immediate priority is to determine time of sx onset (critical for tPA eligibility; must be within 3-4.5 hrs)

• Imaging stu\dies

  • Noncontrast CT or MRI (FIRST TEST)

  • CT angiography (CTA)

  • MRI/MRA)

• Cardiac assessment

  • ECG, echocardiography

  • Cardiac markers (e.g. troponin + BNPs)

  • Many strokes are caused by cardiac embolic

• Blood tests

  • CBC, Plts

  • Coagulation studies (PT/PTT)

  • Electrolytes, glucose

  • Lipid profile

  • Renal and hepatic function

• Lumbar puncture (if suspect SAH but CT is negative)

  • Look for signs of xanthochromia in CSF to indicate old blood/BRB)