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Medicine year 4 CDM > Case 7: spinal cord compression and stroke > Flashcards

Case 7: spinal cord compression and stroke Flashcards

1
Q

ASA

A
  • Caused by stroke of anterior spinal arteries supplying the spinal cord i.e. a spinal cord infarct
  • Tracts affected: Lateral corticospinal tracts, lateral spinothalamic tracts
  • Clinical: bilateral spastic paresis, bilateral loss of pain and temperature sensation
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2
Q

Syringomyelia

A
  • Tracts affected: ventral horns, lateral spinothalamic trar
  • Clinical notes: Flaccid paresis (affects intrinsic hand muscles), loss of pain and temperature sensation
  • Cape like effects upper limbs first
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3
Q

Brown sequard syndrome (spinal cord hemisection)

A
  • Tracts affected: Lateral corticospinal tract, dorsal column, lateral spinothalamic tract
  • Ipsilateral spastic paresis below lesion
  • Ipsilateral loss of proprioception and vibration sensation
  • Contralateral loss of pain and temperature sensation

In any Spinal disease investigate with MRI

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4
Q

Spinal cord metastasis presentation

A
  • Unrelenting lumbar back pain
  • Any thoracic or cervical back pain
  • Worse with sneezing, coughing or straining
  • Nocturnal
  • Associated with tenderness
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5
Q

Types of spinal cord stenosis

A
  • Central stenosis– narrowing of thecentral spinal canal
  • Lateral stenosis– narrowing of thenerve root canals
  • Foramina stenosis– narrowing of theintervertebral foramina
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6
Q

Spinal cord stenosis: symptoms and definition

A
  • Spinal stenosis refers to narrowing of the spinal cord. Can compress spinal cord or nerve roots
  • Symptoms: lower back pain, buttock and leg pain, leg weakness, intermittent neurogenic claudication
  • If severe compression can present with cauda equina, if mild compression can have subtle symptoms
  • Symptoms are absent at rest but occur when standing or walking. Bending forward improves symptoms, standing straight worsens
  • Tend to be more gradual onset
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7
Q

Causes of spinal cord stenosis

A
  • Congenitalspinal stenosis
  • Degenerative changes, including facet joint changes, disc disease and bone spurs
  • Herniated discs
  • Thickening of theligamenta flavaorposterior longitudinal ligament
  • Spinal fractures
  • Spondylolisthesis(anterior displacement of a vertebra out of line with the one below)
  • Tumours
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8
Q

Frontal lobe lesions

A

Frontal lobe = responsible for motor skills, language, intellect, memory and behaviour

Lesion symptoms:
- speech impairment (Broca’s damage in the inferior frontal)
- loss of motor activity
- behavioural changes
- absence of sense of smell

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9
Q

Temporal lobe lesions

A

Temporal lobe = responsible for hearing, memory and speech

Lesion symptoms:
- memory problems
- disruption in the senses
- speech and language disorders
- behavioural changes (Wernicke’s damage in the superior temporal)

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10
Q

Parietal lobe lesions

A

Parietal lobe = responsible for somatosensory detection, pressure and pain

Lesion symptoms:
- loss of somatosensory perception
- asterognosis
- poor language development

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11
Q

Occipital lobe and Dorsal column lesion

A

Occipital lobe lesions: responsible for vision. Lesion symptoms- visual changes

Dorsal column lesion= Ipsilateral loss of fine touch, vibration and proprioception sensation (fibres decussate in the medulla oblongata)

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12
Q

Anterolateral system lesion

A
  • Consists of the anterior and lateral spinothalamic tract
  • Anterior = crude touch and pressure
  • Lateral= pain and temperature
  • Lesion therefore results in impaired pain and temperature sensation on the side contralateral to the lesion (fibres decussate within the spinal cord)
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13
Q

Brown sequard syndrome

A
  • Hemisection of the spinal cord i.e. one sided lesion
    Involving both the DCML and the anterolateral system
  • DCLM = ipsilateral loss of touch, vibration and proprioception
    Anteriolateral system = contralateral loss of pain and temperature sensation
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14
Q

Spinocerebellar lesion

A
  • Ipsilateral loss of muscle coordination - leading to ataxia
  • This is because the spinocerebellar system feeds back to the cerebellum on proprioceptive information in order to aid balance and fine movement
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15
Q

Stroke

A

A clinical syndrome of presumed vascular origin characterised by rapidly developing signs of focal or global disturbance of cerebral functions which lasts longer than 24 hours or leads to death.

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16
Q

Ischaemic and Haemorrhagic stroke

A

Types of stroke- Haemorrhagic (15%), Ischaemic (85%)

Ischaemic- due to occlusion of arteries of cerebral circulation, normally due to an embolism as a result of atrial fibrillation

Haemorrhagic- a collection of blood from a blood vessel rupture.

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17
Q

Types of cerebrovascular disease

A

In order of importance: Ischaemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, undefined disease

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18
Q

Stroke risk factors

A
  • Ischaemic heart disease
  • Peripheral arterial disease
  • Carotid atherosclerosis -> carotid stenosis
  • TIA
  • Vascular heart disease and heart failure
  • Clotting disorders
  • Atrial fibrillation
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19
Q

Stroke symptoms

A
  • Sudden onset
  • F- face may have drooped to one side
  • A- weakness or numbness in one arm
  • S- speech may be slurred or cant speak
  • T- call 999 immediately

Exclude hypoglycaemia in people with sudden onset neurological symptoms as the cause

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20
Q

Stroke investigations

A
  • CT head within an hour
  • CT angiogram of the basilar artery: to recognise brainstem or posterior circulation stroke
  • Check blood pressure to look for hypertension
  • ECG to look for atrial fibrillation (AF)
  • Blood tests in order to check lipids, blood sugar, FBC and clotting
  • Carotid duplex ultrasound to look for atherosclerotic plaque if its an anterior circulation stroke
  • Echocardiogram to check for a clot in ventricles caused by AF
  • Diagnose with ROSIER score
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21
Q

Stroke thrombolysis treatment

A
  • Recombinant Tissue Plasminogen Activator- rTPA (alteplase)
  • 9mg/kg (max 90mg)- 10% bolus and 90% infusion over 1 hour
  • Medically: tPA (intravenous tissue plasminogen activator)
  • NIHSS >4
  • Administer within 4.5 hrs
  • The earlier tPA is administered, the higher the likelihood of a positive neurologic outcome
  • Activates blood clot removal system, restores blood supply, reducing the number of dead neurons
  • Adverse outcome- intracerebral haemorrhage
22
Q

Absolute contraindications for tPa

A
  • Major surgery in last 14 days
  • GI or urinary tract bleeding in last 21 days
  • Stroke < 3 months ago
  • Platelets <100
  • Symptoms suggestive of subarachnoid bleed (even if CT Head clear)
  • BP greater than >185 systolic or >110 diastolic unresponsive to medical treatment
  • INR >1.7 or NOAC (novel oral anticoagulant) within 24-48 hours
23
Q

Endovascular treatment for stroke

A

The clot is caught in a stent and removed, used for moderate to severe stroke when there is large vessel occlusion. Must be administered within 6 hours, can follow tPa or be done when its contraindicated.

24
Q

Relative exclusion criteria for EVT

A
  • Minor stroke symptoms or rapidly resolving symptoms
  • Major surgery or trauma in the last 14 days
  • GI or GU bleeding in the last 21 days
  • MI in last 3 months
  • Seizure at onset of stroke symptoms
  • Pregnancy
25
Q

Stroke medication

A
  • Aspirin (300mg daily) for two weeks, offer a PPI as well if they have dyspepsia
  • Clopidogrel (600mg)
26
Q

Stroke anticoagulants and driving

A

DVLA states no driving for a month after a stroke

Stop anticoagulation treatment in people with haemorrhagic stroke. Reverse the effects of warfarin through prothrombin complex concentrate and intravenous vitamin K.

27
Q

TIA (transient ischaemic attack)

A
  • Transient (less than 24 hours) neurological dysfunction caused by focal brain ischaemia without evidence of acute infarction. Tends to last less than an hour.
  • Give aspirin (300mg daily)
  • MRI can show extent of ischaemia
  • Don’t offer urgent CT
  • Investigation: MRI brain in particular diffusion weighted (DWI) and blood sensitive (SWI) sequences
28
Q

History of TIA

A
  • Symptoms consistent with ‘stroke syndrome’ and depend on arterial territory involved: numbness, weakness, visual loss
  • Abrupt onset, gradual offset
  • Headache may occur
  • Vascular risk factors
  • More common in men, older age
  • Biggest risk factor is hypertension
29
Q

3 main causes of TIA

A
  • Large artery atherosclerosis: in extracranial and large intracranial arteries, ischaemia can occur through embolism or reduction of flow. Detected through doppler and CT/MR angiography
  • Cardioembolism: caused by cardiac disease. Detected through 12 lead ECG, prolonged monitoring and echocardiogram
  • Intracranial small vessel disease: occlusion of small penetrating arteries which result in lacunar infarcts. Diagnosed by CT/MR imaging
30
Q

Investigations for TIA

A
  • FBC, ESR, LFTs, Lipids, HbA1c, TSH, Coagulation Profile
  • Brain Imaging (MRI Brain)
  • Extracranial Vessel Imaging (Carotid Doppler)
  • ECG +/- Cardiac Imaging (Echo)
31
Q

Management of TIA

A
  • Control of BP (<130/80)
  • Antiplatelets (clopidogrel 75mg)
  • Cholesterol reduction (atorvastatin 20-80mg)
  • Lifestyle advice (smoking cessation, dietary advice)
  • Urgent carotid endarterectomy: For those with symptomatic carotid artery stenosis 50-99% should be urgently referred and assessed
  • Oral anticoagulation: DOAC for patients with CHADSVASC risk score 2 or above. Consider bleeding risk- ORBIT or HAS-BLED
32
Q

Risk factors for stroke

A
  • Hypertension
  • Old age: biggest non-modifiable
  • Diabetes, obesity and smoking
  • Vasculopathies, hypercoagulable state
33
Q

Cervical artery dissection

A
  • Biggest cause of stroke in young people
  • Risk factors: hypertension, migraine with aura, cervical trauma (can be trivial), recent infection
  • Often presents with pain
  • Investigation: CT or MRI of cervical vessels
  • Treatment: anticoagulants and antiplatelets
34
Q

Cerebral venous sinus thrombosis (CVST)

A
  • Rare, tends to occur in young sdults especially women between 20-35
  • Typical patient: you women presenting with headache and stroke like symptoms. Prothrombotic tendency such as COCP use. Local infection like sinusitis. Dehydration or widespread malignancy. Can develop seizures
  • Diagnosis: urgent CT venography or MRI
  • Treatment: anticoagulation (Heparin and then warfarin to achieve INR 2-3)
35
Q

What forms the circle of willis

A
  • Internal Carotid Artery
  • Anterior, Middle and Posterior Cerebral Arteries
  • Anterior and Posterior Communicating Arteries
  • Basilar Artery (Vertebral and Superior and Anterior Inferior Cerebellar Arteries)
  • (Posterior Inferior Cerebellar Arteries come off the Vertebral Arteries)
36
Q

Malignant Middle cerebral artery syndrome

A

Suspect in younger ischaemic stroke patients where its a large MCA territory infarct and can cause significant oedema. May need a craniotomy to decompress the brain

37
Q

Why is it important to treat a stroke quickly

A
  • Nerve cells and tissues are lost as rapidly as the stroke progresses
  • The ‘penumbra’ is the endangered and salvageable brain tissue that will become ischaemic if untreated and gradually infarct
38
Q

Total anterior circulation syndrome (TACS)

A
  • Unilateral weakness (and/or sensory deficit) of the face, arm and leg
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphasia, visuospatial disorder)
39
Q

Partial anterior circulation stroke (PACS)

A

Twoof the following need to be present for a diagnosis of aPACS:
- Unilateral weakness (and/or sensory deficit) of the face, arm and leg
- Homonymous hemianopia
- Higher cerebral dysfunction (dysphasia, visuospatial disorder)

40
Q

Posterior circulation syndrome (POCS)

A

Oneof the following need to be present for a diagnosis of aPOCS:

  • Cranial nerve palsy and a contralateral motor/sensory deficit
  • Bilateral motor/sensory deficit
  • Conjugate eye movement disorder (e.g. horizontal gaze palsy)
  • Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
  • Isolated homonymous hemianopia
  • Due to occlusion of vertebral, basilar, cerebellar or PCA vessels
41
Q

Lacuanar stroke (LACS)

A

Oneof the following needs to be present for a diagnosis of aLACS:

  • Pure sensory stroke
  • Pure motor stroke
  • Sensori-motor stroke
  • Ataxic hemiparesis
  • Clumsy hand dysarthia
42
Q

What different arteries cause stroke symptoms

A
  • ICA: aphasia, contralateral motor/sensory loss, ipsilateral eye deviation
  • MCA: aphasia, contralateral motor/sensory loss
  • ACA: aphasia, disinhibition, conjugate eye deviation, contralateral motor/sensory loss
  • PICA: Horner syndrome, ipsilateral palatal weakness, ipsilateral limb ataxia, decreased pain/temperature in contralateral side
  • AICA: ipsilateral deafness, ipsilateral facial motor/sensory loss, ipsilateral limb ataxia, decreased pain/temperature in contralateral body
  • Basilar: altered consciousness, oculomotor abnormalities, facial paresis, ataxia
43
Q

How different strokes affect prognosis

A
  • TACS: more likely to die during admission or the following month, longer hospital stay, more complications (respiratory tract infections) and have long term disability
  • POCS: higher risk of stroke recurrence within first 6 months
44
Q

Initial management in stroke

A
  • Calculate ROSIER score
  • Refer to acute stroke unit: can perform acute reperfusion therapies like IV thrombolysis (ischaemic stroke) and hemicraniectomy
  • Thrombolysis- can give Alteplase within 4.5 hours of onset and haemorrhage has been excluded by CT
45
Q

Common contraindications to alteplase

A
  • Use of anticoagulants within 24 hours prior to stroke (unless INR 1.7 or less if on Warfarin)
  • Hypertension >185/110 despite active lowering
  • Platelets < 100 x109 /l or bleeding tendency
  • Previous history of intracranial bleed
  • Recent history of Ischaemic Stroke or major surgery
  • Trivial, non-disabling or rapidly resolving symptoms
  • Uncertainty over symptom onset i.e. wake up strokes. Onset time is the last time the patient was well or seen well
46
Q

NIHSS score for stroke severity

A
  • No stroke: 0
  • Minor stroke: 0-4
  • Moderate stroke: 5-15
  • Moderate to severe stroke: 16-20
  • Severe stroke: 21-42
47
Q

Interventional radiology and stroke

A
  • Alteplase is not very effective in proximal large artery occlusions (LAO)
  • Proximal LAO effect: the terminal part of the ICA, proximal MCA and Basilar artery. Diagnosed by CT angiography and MR angiography
  • Medical thrombectomy removes these obstructing clots with a clot retrieval device
48
Q

Medicines after stroke

A
  • Start 300mg Aspirin asap and within 24h
  • This is continued for2 weeks OD or until discharge
  • Where alteplase is used, CT 24 hours post-alteplase is needed to exclude haemorrhagic transformation. If excluded, aspirin 300mg can be started
  • Long term treatment after is 75mg Clopidogrel OD
49
Q

Malignant MCA infarction

A
  • A total anterior circulation infarct due to progressive neurological deterioration due to progressive oedema, raised intracranial pressure and cerebral herniation
  • Occurs in a small proportion of <60 patients
  • Were previously fit with little evidence of brain atrophy
  • Treatment: decompressive craniectomy
50
Q

Haemorrhagic stroke

A
  • Where bleeding occurs from an arterial source into the parenchyma
  • Thrombolysis is a major risk factor
  • Main causes: Hypertension and cerebral amyloid angiopathy
  • MRI supports diagnosis based on modified Boston criteria
  • With bleed importance to stabilise ICH volume and prevent haematoma expansion which can be seen on serial CT scans
51
Q

Treatment for Haemorrhagic stroke

A
  1. Rapid anticoagulation reversal (10-20% patients are on anticoagulant)
  2. Intensive Blood Pressure lowering to systolic 130-140mmHg for patients arriving within 6 hours with systolic >150mmHg
  3. Care Pathway involving immediate referral to neurosurgery for all patients with good premorbid function (usingmodified Rankin scale) and any of: GCS <9, posterior fossa ICH, obstructed 3rd or 4th ventricle, haematoma volume >30ml

Medicine year 4 CDM (44 decks)

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