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Neurological, neuromuscular and musculoskeletal disease > PBL 44 > Flashcards

PBL 44 Flashcards

1
Q

What are the two main types of stroke?

A

ischaemic & haemorrhagic

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2
Q

Give some causes of ischaemic strokes

A

Thrombosis
Embolism
Systemic hypoperfusion
Cerebral venous sinus thrombosis

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3
Q

Give some causes of haemorrhagic stroke

A

Cerebral haemorrhage

Subarachnoid haemorrhage

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4
Q

What is the right hemisphere involved in?

A

Creativity, imagination, recognition and emotion

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5
Q

What is the left hemisphere involved in?

A

Logic, number skills, language and analytical skills

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6
Q

Effects of stroke in the cerebellum

A

VANISH’D

  • Dizziness
  • Headache
  • Nausea and vomiting
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7
Q

Effects of stroke in the brainstem

A
  • Breathing and heart functions
  • Body temperature control
  • Balance and coordination
  • Weakness or paralysis
  • Chewing, swallowing, and speaking
  • Vision
  • Coma
  • Death
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8
Q

Signs and symptoms of stroke

A
  • Sudden weakness or paralysis on one side of the body
  • Sudden loss of sensation or abnormal sensations on one side of the body
  • Sudden difficulty speaking, including difficulty coming up with words and sometimes slurred speech
  • Sudden confusion, with difficulty understanding speech
  • Sudden dimness, blurring, or loss of vision, particularly in one eye
  • Sudden dizziness or loss of balance and coordination, leading to falls
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9
Q

Difference between stroke and TIA

A

TIA symptoms usually disappear within minutes and rarely last more than 1 hour

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10
Q

Risk factors for stroke (modifiable and non-modifiable)

A
  • Non-modifiable
    1. Age: older
    2. Gender: male
    3. Race
    4. FHx
    5. Previous strokes
  • Modifiable
    1. Hypertension
    2. Diabetes
    3. AF
    4. Smoking
    5. Hyperlipidaemia
    6. Obesity
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11
Q

Treatments of ischaemic stroke

A

Antiplatelets - CLOPIDOGREL

Anticoagulants - DABIGATRAN (II), APIXABAN(Xa), WARFARIN

Hypertension drugs (Acei, ARB, CCblocker)

Thrombolysis = clot buster

Thromboectomy = widen a narrowed artery

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12
Q

Treatments of haemorrhagic stroke

A

Treatments that help blood clot = Vit K & transfusions of fresh frozen plasma or platelets

Hypertension drugs if needed

Surgery to remove large areas of accumulated blood or shunt to relieve increased ICP

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13
Q

Dysarthria vs dysphasia

A

Dysarthria is caused by UMN lesions of the cerebral hemispheres, or LMN lesions of the brainstem. Affects the bulbar muscles which are used in forming words, so it is a disorder of SPEECH

Dysphasia is a disorder of LANGUAGE. It is the impaired ability to understand or use the spoken word, caused by a lesion in the dominant hemisphere.

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14
Q

Causes of aphasia

A

Stroke
Severe head injury
Brain tumour
Progressive neurological conditions e.g. dementia

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15
Q

Give some means of primary stroke prevention

A

MANAGE THE RISK FACTORS WHEN THERE IS NO PREV. HISTORY

  • Hypertension
  • Smoking cessation
  • Diabetes
  • Dyslipidaemia
  • AF
  • Postmenopausal HRT
  • Diet and exercise
  • Weight
  • Alcohol consumption
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16
Q

Explain secondary stroke prevention

A 
WHEN IS PREV. STROKE HISTORY = ABCDE
A - Antiplatelets and anticoagulants
B - Blood pressure
C - Cessation of smoking, cholesterol lowering medications and carotid revascularisation
D - Diet
E - Exercise
17
Q

Mechanism of clopidogrel

A

ADP receptor inhibitor

ADP causes platelet aggregation

18
Q

Anticoagulants vs antiplatelet function

A

Anticoagulants slow down clotting by reducing fibrin formation (DABIGATRAN, WARFARIN)

Antiplatelets prevent platelets clumping and prevent clots from forming and growing (CLOPIDOGREL/ASPIRIN)

19
Q

How do anterior cerebral infarct symptoms compare to middle cerebral and posterior cerebral?

A

Anterior cerebral = contralateral limb weakness and contralateral sensory deficit where the LOWER LIMB IS MORE IMPACTED

Middle cerebral = contralateral limb weakness and contralateral sensory loss where the UPPER LIMB IS MORE IMPACTED

Posterior cerebral = contralateral problems with vision (homonymous hemianopsia) and also contralateral hemiparesis and sensory deficits

20
Q

Clinical response to brain injury

A
  1. Altered conscious level
    - Loss of consciousness
    - Post traumatic amnesia
  2. Symptoms
    - Vomiting
    - Pain
    - Dizziness
21
Q

Difference between primary and secondary brain injury?

A

Primary = occurs at the moment of trauma

Secondary = occurs immediately after and produces effects which last for a long time

22
Q

Brain injury can be classified as focal or diffuse, what is the difference?

A

Focal = specific location: contusion or haemorrhage

Diffuse = over a widespread area: diffuse axonal injury, hypoxic brain injury, diffuse brain swelling

23
Q

Symptoms of primary brain injury

A

Mechanoporation

Calcium influx

Oxygen free radical formation and lipid peroxidation

Axotomy

Cytokine-mediated inflammatory response

24
Q

Symptoms of secondary brain injury

A
  • Raised ICP
  • Hypoxic brain injury
  • Ischaemic brain injury
  • Seizures
  • Infection
  • Hydrocephalus (>fluid in the brain)
  • Cerebral oedema
  • Excitatory amino acids (EAAs) - Can cause swelling, vacuolization and neuronal death
  • Endogenous opioid peptides - Modulate the presynaptic release of EAA neurotransmitters
25
Q

What is the normal ICP?

26
Q

What is the Monro-Kellie hypothesis?

A

The pressure-volume relationship between ICP, CSF volume, blood, brain tissue and cerebral perfusion pressure

  • It states that the cranial compartment is incompressible and the volume inside the cranium is a fixed volume. The principal buffers for increased volumes include CSF and to a lesser extend blood volume. These buffers respond to increases in volume of the remaining intracranial constituents
  • There comes a point ‘Point of decompensation’ whereby the ability to compensate is LOST, so as the haematoma grows, the ICP will rise and exponentially, until herniation of the brain occurs.
  • The contents of the skull are venous volume, arterial volume, the brain, and CSF. If we add another mass, such as a haematoma, which increases in size (increasing the ICP), there are compensatory mechanisms whereby CSF will leave the skull through systems and ventricles into the CSF spaces of the spine until the ICP is equalised
  • The final pathway from which someone will die from an intracranial haematoma is herniation of the brainstem through the foramen magnum
27
Q

Symptoms which suggest a rise in ICP?

A
  • Headache
  • Vomiting without nausea
  • Ocular palsies
  • Altered level of consciousness
  • Back pain
  • Papilloedema
28
Q

The dorsal column medial lemniscus system is involved in which sensory functions? Where does it decussate and in which situations does it travel to the gracile fasciculus vs the cuneate fasciculus?

A

Fine touch, pressure, vibration, proprioception
Decussates in the medulla
Gracile = below T6 (inner) & Cuneate = above T6 (outer)

29
Q

The spinocerebellar tracts are involved in which sensory functions? Where do they decussate and where do they synapse?

A
  • Proprioception to cerebellum
  • Ipsilateral - Posterior stay ipsilateral, anterior decussate twice (anterior white commisure, superior cerebellar peduncle)
  • Synapse in clarke’s nucleus (posterior grey horn)
  • Travel to cerebellum
30
Q

The spinothalamic tracts are involved in which sensory functions? Where do they decussate and where do they synapse?

A
  • Pain, temperature, crude touch
  • Contralateral - Decussate in spinal cord (2-3 levels above entry)
  • Synapse in posterior horn and thalamus
  • Travel to primary sensory cortex
31
Q

The UMN can be classified based on the region of synapse in the anterior horn, what are the two possibilities?

A

Ventromedial: posture, girdle, muscles

Dorsal lateral: distal movement, fine movement

32
Q

What is the pyramidal UMN tract known as? It is involved in which motor functions? Where does it decussate and where do they synapse?

A
  • It is the corticospinal tract
    • Voluntary skilled motor activity
    • Contralateral - 90% decussate in medulla (lateral), 10% decussate in spinal cord (anterior)
    • Dorsal lateral
    • Lateral controls distal movement, anterior controls proximal movement
33
Q

What are the other extrapyramidal UMN tracts?

A

Vestibulospinal
Tectospinal
Reticulospinal
Rubrospinal

34
Q

Explain the function, route and synapse of the vestibulospinal tract

A
  • Balance, posture
  • Ipsilateral
  • Ventral medial
35
Q

Explain the function, route and synapse of the tectospinal tract

A
  • Orientation, flinching, navigational
  • Contralateral
  • Ventral medial
36
Q

Explain the function, route and synapse of the reticulospinal tract

A
  • Large movements of trunk and limbs
  • Ipsilateral
  • Ventral medial
37
Q

Explain the function, route and synapse of the rubrospinal tract

A
  • Distal arm and hand movement
  • Contralateral
  • Dorsal lateral

Neurological, neuromuscular and musculoskeletal disease (36 decks)

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