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PHTY314 > Week Four > Flashcards

Week Four Flashcards

0
Q

What is a transient ischaemic stroke

A

Lasts less than 24 hours
TIA of the brain or eye is a clinical syndrome characterised by an acute loss of focal brain or monocular function lasting less than 48 hours

Due to a brief period of inadequate blood supply

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1
Q

What is the definition of a stroke and what are the two main things it’s due to

A

Acute loss of focal brain function lasting more than 48 hours
Due to:
- spontaneous haemorrhage into or over the brain substance -haemorrhagic stroke
- inadequate blood supply to a part of the brain as a result of low blood flow, thrombosis, embolism - ischemic stroke/cerebral infarct

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2
Q

Who does stroke affect

A

1/4 < 65yrs

1/2 < 75yrs

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3
Q

Pathogensis of a haemorrhagic stroke

A 
10-15% of all strokes 
Arterial disease
Raised blood pressure
Bleeding diathesis 
Haemorrhagic transformation of an infarct
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4
Q

Pathogensis of an ischaemic stroke

A 
75-80% of all strokes
Large artery thromboembolism 
- extra cranial (40-45%) or intracranial (5-10%)
Small artery disease (20-25%)
Embolism from heart (20%)
Non athermatous arterial disease (5%)
Blood disease (<5%)
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5
Q

What is tPA

A

Tissue plasminogen activator
Thrombolytic medication, must be given within 4 hours of the stroke
~40% of patients are eligible
They are used to help discover the clot quickly and help limit stroke damage and disability

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6
Q

What are the four types of stroke

A

TACS - total anterior circulation syndrome (20%) both MCA and ACA
PACS - partial anterior circulation syndrome (30%) either MCA or ACA
LACS - Lacunar syndrome (25%) blockage of small, deep penetrating arteries
POCS - posterior circulation syndrome (25%) PCA

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7
Q

ACA vs MCA vs PCA

A

ACA - cognitive and LL
MCA - UL and face
PCA - visual and sensation of where you are

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8
Q

What are risk factors for a stroke

A

Previous TIA/stroke
Diabetes
EtOH abuse - alcohol
Ischaemic HD
Atrial fibrillation - irregular heart beat,twitching of atria rather than smooth tectonic contraction
Hypertension
Smoking - nicotine causes vessels to constrict, increasing BP
Drug abuse
Valvular heartiness
Carotid stenosis - narrowing of artery
Arteritis - inflammation of walls of artery

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9
Q

Motor symptoms of a stroke

A

Hemipenes is
Simultaneous bilateral weakness
Difficulty swallowing (dysphasia)
Imbalance

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10
Q

Speech or language disturbance (focal neurological and ocular symptoms)

A

Receptive dysphasia
Expressive dysphasia
Dyslexia
Dysarthria

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11
Q

Sensory symptoms (focal neurological and ocular symptoms)

A

Hemisensory loss
Sensory inattention
Astereognosis - define something by fear

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12
Q

Visual symptoms (focal neurological and ocular symptoms)

A 
Monocular blindness - due to demyelination 
Hemianopia - impacts optic lobe
Quadrantanopia 
Diplopia - blurry/double vision
Bilateral blindness
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13
Q

Vestibular symptoms (focal neurological and ocular symptoms)

A

Vertigo - true spinning not dizziness

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14
Q

Motor planning problems (focal neurological and ocular symptoms)

A

Apraxia - inability to execute learned purposeful movements
Ideational - loss of ability to conceptualise, plan and execute the complex sequence of motor actions
Ideomotor - inability to correctly

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15
Q

Behavioural/cognitive/perceptual symptoms (focal neurological and ocular symptoms)

A

Attention
Memory
Visuospatial
Geographic disorientation

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16
Q

What are some non-focal neurological symptoms

A 
Generalised weakness/sensory loss
Light-headed
Faintness
Blacking out 
Confusion 
Incontinence
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17
Q

TACS is a combination of what

A

Hemipenesis +/- sensory deficit involving 2 of the 3 body parts - face, arm and leg
Homonymous visual field defect
Higher cerebral/cortical dysfunction - dysphasia or neglect or visual-spatial-perceptual problems

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18
Q

What can cause TACS

A

Argue infarct in cerebral cortex, BG or internal capsule
Due to MCA or ACA infarct

Or

Large cerebral haemorrhage in lobes of one hemisphere or in BG

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19
Q

PACS

A

2 of the 3 components of TACS
Or
Higher cortical dysfunction such as dysphasia
Or
Proprioceptive loss in one limb
Or
Motor/sensory deficit restricted to one body area

Note: sensory loss means neglect, but if they have a sensation - dysfunction of perception to sensation means inattention

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20
Q

Causes of PACS

A

Occlusion of a branch of the MCA or trunk of the ACA

21
Q

What are the four main types of lucunar syndrome - LACS

A
  • pure hemi-motor loss involving 2 out of 3 motor areas
  • pure hemi-sensory loss
  • hemisensorimotor loss in 2 of the 3 with no other symptoms
  • ataxic hemiparesis - usually dysarthria and clumsiness in one hand
    I.e. No visual, no cortical, no impaired contraction, no brainstem involvement
22
Q

What are some symptoms and signs of POCS

A 
Dysfunction of the brainstem, cerebellum, thalamus, occipital lobe 
Symptoms: 
- diplopia (abnormal alignment of the eyes)
- vertigo
- facial sensory loss 
- Horner's syndrome
- bilateral weakness/sensory loss
- cerebellar signs

Locked in syndrome

23
Q

What is Horner’s syndrome

A

Sympathetic innervation of the eye
Interruption if sympathetic innervation of the eye causes Horner’s syndrome - such as carcinoma of apex of lungs, neck malignancy, brachial plexus lesion, carotid artery lesion, brainstem lesion

Lead to partial ptosis (impaired or dim vision), constricted pupil retracting, lack of sweating

24
Q

Why can Horner’s syndrome get mixed up with CN III lesion

A

Because there is ptosis and abnormal pupil can be confusing
CN III has similar features - strabismus and diplopia, ptosis, dilation of the pupil, downward abducted RE and inability to accommodate RE

CN III - converges eye so you can squint, raises eyelid and contracts pupil

25
Q

What does the pattern of facial weakness tell you about a stroke

A

Stroke is an UMNL so will have opposite side of face affected

26
Q

What does the anterior limb of the internal capsule do

A

Fibres interconnecting the anterior nucleus and the cingulate gurus, and the mediodorsal nucleus and the prefrontal cortex

27
Q

Posterior limb of the internal capsule

A

Fibres interconnecting VA and VL with motor and premotor cortex
Corticospinal and corticobulbar fibres
Somatosensory fibres from VPL/M to postcentral gyrus

28
Q

What is the genu in the internal capsule for

A

Transition zone

29
Q

Retrolenticular of the internal capsule

A

Thalamus and posterior of cortex (e.g. Parieto-occipital-temporal association cortex and LP/pulvinar; proportion of optic radiation carrying information about inferior visual fields)

30
Q

Sublenticular of internal capsule

A

The remainder of the optic radiation carrying information about the superior visual fields; also auditory radiation

31
Q

What is the limbic system concerned with

A
  1. Emotions important to survival
  2. Visceral responses to these emotions
    Drive-related activities imp that for survival (feeding, territory defence, sex)
32
Q

Transmission of visual information

A

Ganglion cells axon from the 4 retinal quadrants converge toward the optic disc and travel in an organised way in the optic nerve

In the chiasm, axons from the nasal halves both cross the midline
I.e. Information from the right half of the visual field from both eyes is carried by the left optic tract

Lateral field crosses, medial field status on the same side

33
Q

General complications of a stroke due to immobility

A 
Respiratory problems/pneumonia 
Pressure sores 
DVT 
PE
Constipation
34
Q

Local complications of a stroke due to weakness

A

Shoulder subluxation/pain
Contratcures
Falls risk

35
Q

Cerebral complications due to brain damage

A

Epilepsy
Thalamic pain
Associated tone and abnormal movement

36
Q

Long term complications of a stroke

A

Further stroke

Related vascular problems MI

37
Q

Risk factors/secondary prevention

A 
Age
HT
Smoking
Diabetes 
AF
IHD
Carotid stenosis (narrowing)
TIA
PVD
Hypercholesterlaemia
Obesity
EtOH
Family history
38
Q

Recurrent stroke

A

2-4% in first month
10-16% in first year
At five years 30% had had a recurrent stroke

40-50% are independent after 12 months

39
Q

Prognosis of survival for a stroke

A

10% at 7 days
30% at a year
60% at five years

40
Q

What are some mechanisms of recovery from a stroke

A 
Results on of swelling in non-damaged cells - start to work again
Axonal and synaptic growth 
Sprouting of new axon terminals 
Changes in dendritic organisation
Altering the effectiveness of synapse 
Unmasking existing synapses 
Strengthening existing pathways
41
Q

Impairments day 1-2 post TACS

A

Drowsy
Inability to swallow
Poor ability to deep breath
No spontaneous cough or on demand
No active movement throughout affected side
Neglecting affected side limbs
Unable to bridge, roll or adjust bed posture

42
Q

Problem list post TACS

A

Risk of aspiration and chest infection
Risk of developing contratcure, loss of ROM
Risk of developing pressure areas
Risk of developing shoulder pain
Reduced conscious state therefore reduced participation in therapy

43
Q

Treatment plan post TACS

A

Goal setting
Chest monitoring - ACBT, cough stimulation
Daily facilitated limb movement through range
Practice bed mobility
Education about care of affected limbs
Sit out in tilt recliner wheelchair when medically stable
Comment rehab in gym whe able

44
Q

What are the types of rehab

A 
Acute rehab
Slow stream rehab 
Domiciliary cafe
Outpatient 
Day hospital 
Community physiotherapy
45
Q

Principles of physiotherapy post stroke

A

Commence rehab ASAP - as soon as they’re safe - can start at bed
Emphasise active learning
Prevent chest and ROM complications
Protect the UL
Encourage them to be in upright postures throughout the day
Team approach - patient centred
Encourage return to normal movement and discourage compensatory movements

46
Q

How do you know when a patient is unable to cope with rehabilitation

A

Severe deficits and unable to learn, shown no improvement

Comorbidities leading to participate in rehabilitation - severe motor stroke with PMHx of severe dementia

47
Q

What are some dangerous situations

A

Vertebral artery dissection (following neck trauma) - this is an unstable condition, don’t move neck quickly
Cerebral oedema with midline shift - increasing ICP causing brain to herniate (coning)
Bleed into brainstem or cerebellum - limited space in these areas any swelling can have a devastating effect
Patients with worsening symptoms, developing headaches
Patient developing decorticates or decerebrate positioning

48
Q

Essential components for sit to stand

A 
Sitting balance 
Foot placement 
Anterior pelvic tilt with trunk extension 
Anterior WS - shank over toe, DF 
Trunk, hip and knee extension 
Standing balance

Need to get patient to edge of bed

49
Q

Essential components of stand to sit

A 
Standing balance 
Posterior tilt to unlock knees
Anterior tilt 
Inclination of trunk forwards as you shift pelvis backwards
Eccentric quads to lower you down 
Hip and knee flexion 
Sitting balance
50
Q

What are some common adaptive strategies for STS

A

Overusing/taking weight through good side
Failure to lean forwards
Not enough quad strength to actually stand up
Don’t bring feet far back enough

51
Q

What is a bariatric patient

A

More than 90kgs

Requires more than one person to transfer

PHTY314 (5 decks)

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