Balance: Standing balance

Endurance: 2 min walk test

Locomotion: 4 m walk test

Strength: grip strength

Dexterity: 9 hole peg test

Nonprogressive disorder of the CNS- Acquired in adolescence or adulthood

Practice Pattern?

Age

Previous stroke Transient Ischimic Attack(TIA)

Fam Hx

Race

Hypertension (HTN)

High cholesterol

Heart Disease

Diabetes

Smoking

Alcohol usse

Overweight

Headache

Weakness or numbness

Trouble speaking

Vision problems

Dizziness, unsteadiness

Follow the progression down from the top: Headache, vision problems, Trouble speaking, Dizzyness, Weakness or numbness

F: Face: is the smile symetrical

A: Arms: does one arm drop down lower than the other

S: Speech: is their speech slurred

T:Time: if person has these symptoms go to the ER

What are the type of CVA and their definitions?

Ischemic: Interuption of blood flow by a blood clot

Hemorrhagic Stroke: Rupture of blood vessels

What artery do the most stroke occur in and what area's does this affect the most.

Why is this the most common artery affected by CVA?

Middle cerebral artery

Face and UE

The middle cerbral artery branches off the corotid artery. Often a clot will be in the corotid and then break off and get stuck in the middle CA

Thrombotic: Clot forms in the cerebral arteries or branches

Embolic: Clot formed elsewhere and traveled

What is the characteristic fo a TIA?

3 layers of Spinal mengies.

1. Dural 2. Arachoind 3. Pia

Tell me about the potiential spaces between the menigies?

What are the bleeds that can occur there?

Subdural space: Subdural hematoma. Cerebral veins tear low presssure slower onset of symptoms. As well as fewer symptoms.

Epidural Space : Epidural hematoma: Menigeal arteries tears and bleed. Increase intercranial pressure= brain stem dysfunction

A subdural hematoma is the result of what?

Do the symptoms occur slow or fast and why?

A tear in the cerebral veins

Symptoms occur slowly bc the veins are low pressure

A epidural hematoma occurs bc of what?

What happens as a result and what can this cause?

This would associated with what kind of stroke?

Menigeal artery tear and bleed.

This causes increase crainal pressure which can place pressure on the brain stem( the cardiorespiratory center)

Headaches can also be a sx

hemorrhagic

IN a hemorrhagic stroke is the bleed controled or uncontroled?

What is the result of this type of bleeding?

Uncontrolled

Increased intercrainal pressure as a result of the distal flooding of blood

What are the two types of hemorrhagic strokes?

what are their characteristics?

Subarachnoid hemorrhage: Aneurysm in walls of large blood vessels (Aneurysm: a widening or buldging of a blood vessel in a spot of weakness)

Intracerebral hemorrhage: Rupture of cerebral blood vessels

What can be some of the structural problems wtih  the blood vessels in the brain?

What is the cause of these structural problems?

Aneurysms: Weaking in blood vessel wall leading to dilation of the vessel

Arteriovenous malformation (AVM): developmental abnomalities with arteries connected to veins by thin walled vessels lead to rupture. There is no capillary connection between the artery and the vein.

Type of stroke

Time elapsed from initial to being seen in the hospital onset

Severity

Age and general status before strokes directly relates to how they will recover

Medical management for stroke: Surgical procedures

what are the surgical procedures and their description?

Decompressive craniotomy: relieves the pressure on the brain by taking out a peice of the skull

Catheter Embolectomy: Run a catheter through the artery to where the clot is and disrupt the clot. Danger is that the clot will become dislogded somewhere else

Carotid endarterectomy: Will cut the internal carotid artery and take out the clot. Risk that part of it will dislodge

Arterial by pass: bi-passing affected vessel

Angioplasty with stent: place deflated balloon in the vessel, inflate it and then place the stent to maintain the opening

To repair blood vessels:

Aneurysm Repair: brain surgery ad clamp blood vessels

catheter with coils to scar blood vessel wall

Medical procedures to treat CVA: Drug therapy

What drugs are used in order to treat a CVA pharmcologically?

Thrombolytic therapy (clot busters):

1. Tissue plasminogen activator (t-PA), really important for ischmic stroke

Anticoagulant (heparin; coumadin)/ Antiplatelet (aspirin) drugs

Medications for HTN, colesterol

What is the time frame that is need in order to administer the drug Tissue plasminogen Activator (t-PA)?

What does this time frame allow the medical professionals to do?

Door to doctor: 10 min

Access to neurological expertise: 15 min

Doort to CT scan: 25 min

Door to CT scann interp.: 45 min

Door to tx: 60 min

Door to CVA unit or ICU: 3 hours

This time frame allow them to determine whether or not they have an ischimic stroke.

What is the criteria for that guides the start of the time line?

What is the time line that guides intervention for a CVA?

The criteria is that is that time on-set is the last time that they were seen normal

0-3 hours: Intravenous tPA

0-6 hours: intra-arterial tPA (a non-FDA aproved therapy)

0-8 hours: mechanical embolectomy

More than 8 hours: Anticoagulants or antiplatelets

Vertebrobasilar Artery (VBA) supplies what part of the brain?

what will be affected if these structures are damaged?

Cerebellum, Brainstem, Medulla, Pons

Balance, coordination, will affect breathing and heart

Contralateral spastic hemiparesis(weakness) and sensory loss

Face and UE are affected more the the LE

(aphasia(lf hemi), perceptual deficits (rt hemi), homonymous hemianopsia (more rt vision))

LE > UE

(Contralateral hemiparesis, sensory loss, urinary incotinences, apraxia (corpus callosum)

Thalamic sensory syndrome (pain)

Homonymous hemiaopsia

Visual agosia( cannot recog object even though sensory system is in tact)

Cortical blindness if bilateral ( damage to visual area of the brain i.e the occipital lobe (calcarine sulcus)

Amnesia (temporal lobe)

Locked-in syndrome: No motor ability but the person is concious. Can feel can move their eyes.

Tetraplegia, preserved consciousness and sensation, vertical (only voluntary movements of the eyes)

Cerebellar and cranialnerve imapairments

Note: CN are not UMN

LCVA: R sided weakness and sensory loose, behavior is slow and catious, aware and axious about their in ability to move, speech and language is affected the most aphasias, difficulty processing verbal cues, apraxia

RCVA: impulsive behavior/poor judgement, diff w/ visual cues, Visual-perceptual issues ( L sided neglect, Agnosia, Body scheme), L sided weakness and sensory loss)

Abnormal synergy patterns, Paresis (weakness), Coordination deficits

Abnormal tone, abnormal reflexes, impaired balance

homonymous hemianopsia

PT do not directly work with this but have to teach them compensatory stratagies.

Contractures (PT responsibility to prevent these), shoulder subluzation/pain.

(shoulder hand syndrome (refles sympathetic dystrophy (RSD) AKA complex regiona pain syndrome))

Neuromuscular, Musculoskeletal, Integumentary

Cardiopulmonary( need to educate them on this, endurance testing is not a bad idea either)

Cognitive/affective: not a system but super important

Oriented to time, place, person

Can start general work to specific

Bed Mobility

Transfers

Locomotion

Flaccidity during acute phase

No movement can be elicited

Some voluntary control of movement synergies

Spasticity has further increased

Movements out of synergies (can be just change in one joint)

Spasticity begins to decrease

More difficult movement combinations

Limb synergies not dominat anymore

Disapperance of spasticity

Individul joint movements and cordination near normal

What other standardized test is the Fugl Meyer based on?

Voluntary movements of the UE and LE

Balance

Sensations

With RGO's what is the energy expense and speed of walking compared with that of normal gait?

What is the discontining rate in childern/adults

10x greater energy expenses

80% slower walking speed

61-90% childern

46-54 in adults

No contractures in the hi pflx,knee flx or ankle PF

Strait leg raise of 0-110 deg

Independent in all transfers including WC to floor

Max Vo2 is >= 20 ml/kg/min

50 continuous full dips in parallel bars

CVA with strength deficits at the knee

CP with strength deficits at the knee

Significant OA or RA impacting knee pain/funct

Femoral nerve palsy

Mid-low level incomplete lumbar SCI or myelomeningocele

When are locking vs not locking unilatearl KAFO's apperoperiate?

What are the key factors?

If pt has knee hyperextension control W/O pain:

Free knee jt if pt has adequate sagittal plane stability

offset knee joint if fatigue can be tolerated, allows extension moment in stance and free motion in swing b/c axis is et posterior to the joint line, causing the pts COM to be anterior to the axis

Key Factors: Pain and stability will be the diffrence in whether they will be in free motion or stance control or no motion

What should be added tot he KAFO if the pt has knee flexion contractures?

WHy is this needed?

Anterior tibial shell

needed to prevent croutching

Low Lumbar/Sacral level SCI or myelomeningocele

CVA

CP with a GMFCS level of II-V

Charcot Marie Tooth syndrome (CMT)

TBI

What would be the indications for a Solid or a locked joint AFO?

What if the indications for for a solid AFO are present but they are mild, is the same choice made?

what if non of the indications are present what do you choose then?

No

Choose articulated  AFO or DAFO w/ PF stop (prevents spasticity from causing a PF)

AFO w/ articulated ankle/DAFO allowing ankle movement

Excess pinching/compression of the limb (causing reported or visible changes inthe skin)

Excess skin breakdown- skin erythema does not disappear in 10-15 min

Too many components are broken or non-functional

Insult to the brain , not degenerative or congenital nature caused by an external force, that may produce a diminished state of consciousness, which results in cognitive impairments or physical functioning

TBI: Trauma to the brain caused by external force, not of degenerative or congenital sources, which produces a lower level of conciousness, which results in impairments in cognition or physical functioning

the #1 killer of young adults?TBI from motor vechicle acidents, sport, falls

15-24 YOG

Men> Women

Motor vehicle acident (51%)

Falls 21%

Assults 12%

Sports 10%

Blow to the head: Coup-contrecoup damage to brain under site of impact and directly opposite site of impact

Penetrating Injuries: Gunshot

Diffuse Axonal Damage: Mild stretch of Axons equals Concussion. Sever stretch or shearing of axons= DAI (i thing diffuse axonal injury?)

Coup-contrecoup: where the brain is damage at the site of impact and then directly opposite the site of impact

Whip-lash

Local

Polar

Diffuse axonal injury

Scattered shearing of subcortical axons

Severe head injury- lidbrain and brainstem affected

Decorticate and decerebrate posturing (this is seen with diffuse axonal shearing showing a higher level brain injury)

Hypoxic-ischemic injury secondary to shifting of brain structures

hematomas(Epidural, subdural, intracerebral)

Increased intracranial pressure (normal ICP: 5-15mmhg)

infection: with a gunshot wound or laceration

Neurochemical changes (autodestrictiv cellular phenomena with DAI) (Increased levels of excitatory neurotransmitters)

Mild TBI

Postconcussion syndrome

Brief loss of consciousness

Loss of memory immediately before? or after the injury

Alteration in mental state at the time of the accident

Focal neurological defivits

Long-term effects of mild TBI

Cognitive and personality changes

Location of injury

Size of injury

Structures involved in the injury

Availability of collateral blood flow

1. premorbid status

2. Type of Primary injury

3. Secondary injury

MRI: hematomas, atrophy, ventricular enlargement, nonhemorrhagic lesions

Cerebral Blood flow (CBF) mapping: Positive emission tomography (PET)

CT and Electroencephalography (EEG) can also be used

Urine analysis

Blood analysis

Echocardiogram

Doppler ultrasound (arterial blood flow)

MAP range is 70-100 mmhg

MAP= (1/3(SBP-DBP)+DBP)

In the acute medical management of TBI what is the range of normal and at what ICP valvue is intevention required ?

IF ICP is two high how can this affect on the Brain?

ICP range normal: 5-15 mmhg

ICP invention: >20 mmhg require intervention to reduce ICP

Increased ICP effect on the brain is to limit blood perfusion to the brain and potiential herniate brain tissue through the forament magnum which will cause cell damage and potientially place the brain stem at risk by placing pressure on it

>70 mmhg (range of 60-90mmhg)

CPP= MAP-ICP

need enough pressure to get blood to the brain

Drugs that poorl penetrate the brain.

bc drugs could place the brain at risk

level of consciousness

Orientation

memory

Problem-solving/reasoning deficits

Perseveration( pt constantly saying one thing cannot get off a idea or topic)

Impaired safety awareness

Impaired executive functioning

Cognitive assessment: how will you assess oreintation?

Level of consciousness

Memory (impacts how you teach them)

Executive Function

Safety/judgement

Sexual disinhibition: (inappropriate comments)

Emotional disinhibition: laughing or crying inappropriate to situation

Aggressive disinhibtion: profanity, hitting

Apathy

Depression

Receptive Aphasia

Expressive Aphasia

Motor speech/dyarthria

Neuromuscular Deficits

Synergy patterns

Sensations

Weakness

Balance

Tone

Functional Assessment of TBI pt includes what?

Balance

Mobility (bed Mob, Transfers, Gait)

ADL

Diability Measures: SF-36: health status measure, Modified Rankin Scale: global functional health indicator.

Functional Assessment: Functional indepence Measure (FIM)

Dynamic Fait Index( DGI)

TBI assessment tools: Rancho Los amigos LOCG