Subarachnoid haemorrhage

Question 1

Why does pain occur in the head?

Answer 1

Occurs when peripheral noiciceptors are stimulated in response to injury (traction, displacement, inflammation, vascular spasm or distension of pain sensitive structures) but can occur when pain producing pathways of the peripheral or CNS are damaged or activated inappropriately.

Question 2

What are some of the mechanisms of cranial pain?

Answer 2

1) Dilation of arteries (eg after seizures/histamine/alcohol
2) Infection or blockage of paranasal sinuses- pain over same distribution (change in pressure)
3) Long or short sightedness
4) Diseases of ligaments, muscles and apophysial joints in upper cervical
5) Meningeal irritation
6) Subarachnoid haemorrhage

Question 3

What are the meninges and what are the characteristics of each?

Answer 3

You should know this…

Question 4

What is the triad of meningism?

Answer 4

Nuchal rigidity, photophobia and headache

Question 5

What is Kernig’s sign?

Answer 5

Lie on back, knee raised and extension of knee is painful

Question 6

Brudzinski’s sign?

Answer 6

forced flexion of the neck towards the chest will cause involuntary flexion of the hips and knees.

Positive: Meningitis, SAH, Encephalitis, Meningism

Question 7

What is an epidural haemotoma?

Answer 7

Lens/concave shaped on scan
Normally the dura is fused with the periosteum on the internal surface of the skull. Dural arteries are vulnerable to injury, particularly with temporal skull fractures in which the fracture lines cross the course of the vessel. Once a vessel has been torn, the extravasion of blood under arterial pressure can cause the dura to separate from the inner surface of the skull. The expanding haematoma has a smooth inner contour that compresses the brain
surface.
When blood accumulates slowly, patients may be lucid for several hours before
onset of neurological signs.
May expand rapidly and is a neurosurgical emergency requiring prompt drainage.
Often traumatic in origin – present with headache or altered consciousness

Question 8

What is a subdural haematoma?

Answer 8

Cresent shaped on scan
Typically, venous bleeding is self-limited. Breakdown and organization of the
haematoma take place over time in the following sequence:Lysis of the clot (1 week), Growth of fibroblasts from the dural surface into the haematoma (2 weeks), Early development of hyalinised connective tissue (1-3 months).
There may be focal signs, but often the clinical manifestations are nonlocalising
and include headache and confusion, altered consciousness.

Question 9

What are the most common causes of aneurysms?

Answer 9

Saccular (75% of SAH), Fusiform (widening of a segment of an artery around the entire blood vessel), mycotic (usually more distal along than berry aneurysms), traumatic, dissecting

Question 10

Where do aneurysms occur?

Answer 10

Middle cerebral 29%, ICA 16%, ACA 15%, Basiliar 14%, PCA and V 6% and PCA 3%

Question 11

How do you investigate a suspected SAH?

Answer 11

CT (most sensitive on the day bleeding occurs and in pts with LOC), then CT
Then 4 vessel cerebral angiography (necessary for surgical tx)

Question 12

What are some possible complications of SAH?

Answer 12

1) Reoccurance of haemorrhage
2) Intraparenchymal extension- produce intracerebral haematoma
3) Arterial vasospasm- lead to ischaemia
4) Acute or subactue hydrocephalus- impaired CSF absorption in SA space
5) Seizures

Question 13

What are the signs and symptoms of a intracerebral/intraparenchymal haemorrhage?

Answer 13

Severe headache and depression of consciouness as well as neurologic deficts that do not correspond to a single blood vessel
Could be caused by: hypertension and cerebral amyloid angiopathy

Question 14

What is the pupillary light reflex?

Answer 14

1. Optic nerve fibres (or their collaterals) to the pretectum, a nuclear area between thalamus and midbrain.
2. Short fibres go from the pretectum (at the superior colliculus) to both Edinger–Westphal nuclei (the visceral components of the
   oculomotor nuclei) by way of the posterior commissure and to both cilliary ganglia by way of the oculomotor nerves.
3. Postganglionic parasympathetic fibres to the constrictor muscles are activated,
   and the sympathetic nerves of the dilator muscle are inhibited

Question 15

What is the accommodation reflex?

Answer 15

CN2 (afferent limb of reflex) -> occipital lobe -> pretectum -> pupil accommodation, lens accommodation, convergence

Question 16

Which CN come off ventrally?

Answer 16

olfactory, optic, oculomotor, abducens, hypoglossal.

Question 17

Which CN come off laterally?

Answer 17

trigeminal, facial, vestibulocochlear, glossopharyngeal, vagus, accessory

Question 18

What does a compression of L CN3 do?

Answer 18

Difficulty opening eye (LPS)
Dilation of left pupil (Spincter papillae)- photophobia
Eye moves down and out

Question 19

What does a compression of R CN4 do?

Answer 19

Eyeball cannot turn inferomedially so diplopia when looking down

Question 20

What does a compression of the CN6 do?

Answer 20

Complete paralysis causes medial deviation and diplopia

Question 21

What are the 3 function categories of brainstem activities?

Answer 21

Conduit functions
Cranial nerve functions
Integrative functions

Question 22

What is the supposed pathogensis of migraine?

Answer 22

Stimulation of the trigeminal ganglion results in release of vasoactive neuropeptides, including substance P, calcitonin gene related peptide, and neurokinin A. release of these neuropeptides results in the process of neurogenic inflammation. Neurogenic inflammation may lead to the process of sensitization. This is the process whereby the stimulus needed to generate a response decreases over time, while the amplitude of the response to any given stimulus increases. The CNS neurons become increasingly responsive to nocioceptive and non-nocioceptive stimulation.
+low 5HT (deficit in inhibitory pain system), Cortical spreading depression,

Question 23

What is the diagnostic criteria of a migraine?

Answer 23

Repeated attacks lasting 4-72 hours with a normal physical and 2 of (unilateral pain, throbbing pain, aggravation by movement, moderate or severe intensity) plus 1 of (nausea/vomiting, photophobia and phonophobia)

Question 24

What is the treatment of a migraine?

Answer 24

Lifestyle modification (decrease stress etc)
1. lie in quiet, darkened room and avoid movement- asprin or NSAID
2.Triptan (5HT1B/1D agonist) 
Opioid analgesics (pethidine)- last resort

Question 25

What characterised a tension type headache?

Answer 25

Chronic head-pain syndrome characterized by bilateral tight, band like discomfort.
Appears to be due to primary disorder of CNS pain modulation alone
Tx: panadol, asprin or NSAIDS but for chronic amitriptyline (tricyclic antidepressant)

Question 26

What are the symptoms of a cluster headache?

Answer 26

Deep, often retroorbital pain, often excrutiating, nonfluctuating and explosive in quality. Core feature: daily bouts of 1/2 for 8-10 weeks and then pain free interval for less than a year.
Pts move about (vs migraine), photophobia, phonophobia, ipsilateral sx of cranial para autonomic activation (crying, runny nose)
Likely to be a disorder involving central pacemaker neurons in the region of the posterior hypothalamus

Question 27

What is the treatment of cluster headache?

Answer 27

Acute: oxygen inhalation, sumatriptan SC and zolmitriptan nasal sprays
Preventative: glucocorticoids (short bouts)
Lithium (chronic) and verapamil (heart block SE)

Question 28

What is temporal arteritis?

Answer 28

(Giant cell) is an inflammatory disorder of the arteries that frequently involves extracranial carotid circulation. Can developo blindness due to involvement of ophthalmic artery so tx with glucocorticoids
Prednisone for 4-6 weeks

Question 29

How do you treat an intracranial haemorrhage?

Answer 29

CT- diagnosis
Medical: elevation of head, mild sedation and analgesics for headache (avoid hypotension), IV fluids used with care, Prophylactic calcium channel antagonist (nimodipine) may help and anticonvulsant is recommended
Surgical: Clipping or coiling

Question 30

What are some possible causes of raised ICP?

Answer 30

extra/cerebral mass, generalised brain swelling, increase in venous pressure, obstruction to the flow and absorption of CSF

Question 31

What are the clinical features of raised ICP?

Answer 31

Headache, nausea, vomiting, drowsiness, altered mental status, diplopia, ocular palsies and papilloedema and Cushing’s triad

Question 32

What is the management of raised ICP?

Answer 32

Elevate head of bed, intubate and hyperventilate (vasoconstriction), mannitol ventricular drainage
If this fails
Barbiturate induced coma, hemicaniectomy, steriods