5- Neurology (Less acute: Brain tumours and stroke) Flashcards

1
Q

presentation of brain tumours

A
  • Often asymptomatic when small
  • Focal neurological symptoms depending on location of lesion
  • RICP
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2
Q

investigation for brain tumour

A

Investigations
- MRI
- CT

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3
Q

Papilloedema

A

Papilloedema is a swelling of the optic disc secondary to raised intracranial pressure. Papill-refers to a small rounded raised area (the optic disc) and -oedema refers to the swelling. The sheath around the optic nerve is connected with the subarachnoid space. Therefore it is possible for CSF under high pressure to flow into the optic nerve sheath. This increases the pressure around the optic nerve where it connects with the back of the eye at the optic disc, causing optic disc swelling. This can be seen on fundoscopy examination.

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4
Q

Fundoscopic Changes

A
  • Blurring of the optic disc margin
  • Elevated optic disc (look for the way the retinal vessels flow across the disc to see the elevation)
  • Loss of venous pulsation
  • Engorged retinal veins
  • Haemorrhages around optic disc
  • Paton’s lines which are creases in the retina around the optic disc
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5
Q

Pituitary Tumours

A

Pituitary tumours tend to be benign. If they grow large enough they can press on the optic chiasm causing a specific visual field defect called a bitemporal hemianopia. This causes loss of the outer half of the visual fields in both eyes. They have the potential to cause hormone deficiencies (hypopituitarism) or to release excessive hormones leading to:
* Acromegaly
* Hyperprolactinaemia
* Cushing’s disease
* Thyrotoxicosis

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6
Q

stroke definition

A

a neurological deficit attributed to an acute focal injury of the central nervous system (CNS) by a vascular cause, including cerebral infarction, intracerebral hemorrhage (ICH), and subarachnoid haemorrhage (SAH)”

also known as a cerebrovascular accident (CVA)

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7
Q

Cerebrovascular accidents are either:

A

Ischaemia or infarction of brain tissue secondary to inadequate blood supply
Intracranial haemorrhage

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8
Q

Disruption of blood supply can be caused by:

A
  • Thrombus formation or embolus, for example in patients with atrial fibrillation
  • Atherosclerosis
  • Shock
  • Vasculitis
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9
Q

Transient ischaemic attack (TIA)

A

was originally defined as symptoms of a stroke that resolve within 24 hours. It has been updated based on advanced imaging to now be defined as transient neurological dysfunction secondary to ischaemia without infarction.

Transient ischaemic attacks often precede a full stroke.

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10
Q

A crescendo TIA is where…

A

is where there are two or more TIAs within a week. This carries a high risk of developing in to a stroke.

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11
Q

presentation of stroke

A

suddent onset neurological symptoms
* Sudden weakness of limbs
* Sudden facial weakness
* Sudden onset dysphasia (speech disturbance)
* Sudden onset visual or sensory loss

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12
Q

Risk Factors of stroke

A

Cardiovascular disease such as angina, myocardial infarction and peripheral vascular disease
Previous stroke or TIA
Atrial fibrillation
Carotid artery disease
Hypertension
Diabetes
Smoking
Vasculitis
Thrombophilia
Combined contraceptive pill

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13
Q

FAST Tool for Identifying a Stroke in the Community

A

F – Face
A – Arm
S – Speech
T – Time (act fast and call 999)

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14
Q

management of stroke

A
  • Admit patients to a specialist stroke centre
  • Exclude hypoglycaemia
  • Immediate CT brain to exclude primary intracerebral haemorrhage
  • Aspirin 300mg stat (after the CT) and continued for 2 weeks

Options if ischaemic stroke - must exclude risk of intracranial haemorrhage
- Thrombolysis
- Thrombectomy

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15
Q

Thrombolysis with

A

Alteplase can be used after the CT brain scan has excluded an intracranial haemorrhage.

  • Alteplase is a tissue plasminogen activator that rapidly breaks down clots and can reverse the effects of a stroke if given in time.
  • It is given based on local protocols by an experienced physician.
  • It needs to be given within a defined window of opportunity (4.5 hours)
  • Patients need monitoring for post thrombolysis complications such as intracranial or systemic haemorrhage.
  • This includes using repeated CT scans of the brain.
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16
Q

strict rules associated with alteplase

A

Clinical diagnosis of ischemic stroke causing neurological deficit

Time of symptom onset <4.5 hours

> 18

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17
Q

Absolute Contraindications to tPA

A

Intracranial hemorrhage on CT

Clinical presentation suggests subarachnoid hemorrhage

Neurosurgery, head trauma, or stroke in past 3 months

Uncontrolled hypertension (>185 mmHg SBP or >110 mmHg DBP)

History of intracranial hemorrhage

Known intracranial arteriovenous malformation, neoplasm, or aneurysm

Active internal bleeding

Suspected/confirmed endocarditis

Known bleeding diathesis
(1) Platelet count < 100,000

18
Q

Thrombectomy

A

(mechanical removal of the clot) may be offered if an occlusion is confirmed on imaging, depending on the location and the time since the symptoms started. It is not used after 24 hours since the onset of symptoms.

19
Q

blood pressure and stroke

A

Generally, blood pressure should not be lowered during a stroke because this risks reducing the perfusion to the brain.

20
Q

Management of TIA

A

Start aspirin 300mg daily. Start secondary prevention measures for cardiovascular disease. They should be referred and seen within 24 hours by a stroke specialist.

21
Q

Specialist Imaging

A

the aim of imaging is to establish the vascular territory that is affected. It is guided by specialist assessment.

1) Diffusion-weighted MRI is the gold standard imaging technique. CT is an alternative.

2) Carotid ultrasound can be used to assess for carotid stenosis. Endarterectomy to remove plaques or carotid stenting to widen the lumen should be considered if there is carotid stenosis.

22
Q

Secondary Prevention of Stroke

A
  • Clopidogrel 75mg once daily (alternatively dipyridamole 200mg twice daily)
  • Atorvastatin 80mg should be started but not immediately
  • Carotid endarterectomy or stenting in patients with carotid artery disease
  • Treat modifiable risk factors such as hypertension and diabetes
23
Q

Stroke Rehabilitation

A

Once patients have had a stroke they require a period of adjustment and rehabilitation. This is essential and central to stroke care. It involves a multidisciplinary team including:

  • Nurses
  • Speech and language (SALT)
  • Dieticians
  • Physiotherapy
  • Occupational therapy
  • Social services
  • Optometry and ophthalmology
  • Psychology
  • Orthotics
24
Q

the frontal lobe

A

LocationAnterior to central sulcus

Major functions
1) Motor
- Primary motor cortex
- Motor homunculus
2) Expression of speech (usually left hemisphere)

3) Behavioural regulation/judgement
- E.g. Phineas Gage story- iron rod went through frontal lobe. Became impulsive, alcoholic and violent behaviour significantly changed

Cognition
- E.g. mathematical ability

Eye movement
- Region called frontal eye field
- Projects down onto the brainstem and communicates with CN nuclei relevant to the eyes

Continence
- Paracentral lobule (near midline)- regulates micturition

25
Q

the parietal lobe

A

Location Posterior to central sulcus

Major functions
1) Sensory
2) Comprehension of speech (usually left hemisphere)
- Wernicke’s area
3) Body image (usually right)
4) Awareness of external environment (attention)
- Condition called Neglect – despite the fact pt has normal visual field, they can’t acknowledge the existent of one of half of their environment
5) Calculation and writing
6) Don’t forget visual pathways projecting through white matter
- Superior optic radiations pass through the parietal lobe

26
Q

the temporal lobe

A

LocationInferior to sylvian fissures

Major functions
1) Sensory (relatively posterior)
- Hearing- primary auditory cortex (superior)
- Olfaction- primary olfactory cortex (inferior)

2) Memory
- Hippocampus sits deep in the temporal love e.g. factual memory

3)Emotion
- Thought olfactory centre (smell) is linked to emotional function

4) Don’t forget visual pathways projecting through white matter
- Inferior optic radiations pass through the temporal lobe

27
Q

Cerebral dominance/ lateralisation

A

Asymmetry in the functions of the left and right cerebral hemispheres
- Left hemisphere is dominant in 95% of people (think about how it controls the right hand)
- Right hemispheres attends to both halves of spaces but the left hemispheres only attends only to the right half of space
o This links to Neglect disorder

28
Q

Left hemisphere

A

Sequential processing (processing which occurs in a serial fashion):
- Language
- Mathematic/logic

29
Q

Right hemisphere

A
  • Whole picture processing:
  • Body image
  • Visuospatial awareness
  • Emotion
  • Music
30
Q

The corpus callosum

A

Allows the left and right hemispheres to work together

A huge bundle of white matter connecting the two hemispheres. An early surgical treatment for severe epilepsy was to cut the corpus callosum to prevent seizure activity from propagating through the whole brain. This had some interesting neuropsychological consequences for those patients…

31
Q

language pathways are dominant in the

A

left hemisphere

32
Q

importa t areas for corrrect processing of language

A

Brocas
Wernickes

33
Q

Brocas area

A
  • Inferior lateral portion (think face of homunculus) of frontal lobe
  • Production of speech (motor function)
  • Directs muscles to produce language
34
Q

Wernickes area

A
  • Superior portion of temporal (some say parietal as well) lobe - near primary auditory region
  • Interpretation of language (sensory)
  • Understanding of what is being said
35
Q

Brocas and Wernickes areas are connected together via

A

Arcuate fasciculus (green)- white matter
- Best though of as a unidirectional pathway (although is technically bilateral)

36
Q

1) Pathway for repeating a heard word

A
  1. Word heard
  2. Auditory info is processed in the cortex within the primary auditory cortex and then goes to Wernicke’s area- where it is interpreted and translated into language
  3. Wernicke’s area then communicates with Broca’s’ area through the arcuate fasciculus
  4. Broca’s area tells the cortex to produce pattern of muscle contractions which will produce the sound of the word that was previously heard
  5. Impulse to primary motor cortex (PMC) area which drives the facial and laryngeal muscles, resulting in repetition of heard word

Damage specially to arcuate fasciculus results in patients not being able to repeat the word

37
Q

2) Pathway for speaking a written word

A
  1. When we read we use primary visual cortex in occipital lobe
  2. Visual pattern sent from visual cortex to Wernicke’s area
  3. Wernicke’s is then able to examine pattern as impulses and interpret pattern as a word
  4. Wernicke’s then sends word via the arcuate fasciculus to Broca’s area
  5. Broca’s area then instructs PMC to produce a pattern of muscular contraction in order to produce pattern of musculature contraction to produce the read word
38
Q

3) Pathway for speaking a thought

A
  1. Thoughts can arise from many brain regions, but converges at Wernicke’s area
  2. Wernicke’s interprets thought patterns and converts into language
  3. Sends impulses to Broca’s via the arcuate fasciculus
  4. Broca’s sends to PMC instructing to produce pattern of musculature contraction to be able to speak thought
39
Q

Wernicke’s aphasia (fluent aphasia)

A

A type of aphasia (language disorder after stroke) with poor comprehension. Speech is effortless, but the meaning is impaired.
- Speech is very fluent and condiment
o Intact Broca’s
- However what they say doesn’t make any sense at all
- Cant understand questions being asked

40
Q

Broca’s aphasia

A

A type of aphasia characterized by partial loss of the ability to produce language (spoken, manual, or written), although comprehension generally remains intact
- No problem with understanding questions being asked
o Wernicke’s area intact
- Frustration with trying to articulate answer
o Hesitant and lots of pausing

41
Q

delete - wernickes aphasia vs wernickes encephalopathy

A

Wernicke’s encephalopathy is a degenerative brain disorder caused by the lack of vitamin B1 (thiamine)

It may result from: Alcohol abuse. Dietary deficiencies. Prolonged vomiting

Presentation
- Ataxia
- Ophthalmoplegia
- Altered mental state