This is a 44 year old previously well female who acutely developed a severe headache and difficulty walking who then, within minutes, lost concisousness. On examination she is comatose with neck stiffness, a positive KernigŐs sign, blood pressure of 180/110, tachycardia, fundi showing venous congestion, full range of dollŐs eyes extraocular movments, no response to verbal stimuli, uttering incomprehensible sounds and opening her eyes to strong pain and moves all 4 limbs to pain with pain localization, although this movement is reduced on the right side (GCS E2, V2, M5)

Summary is too long.

This is a 44 year old female with sudden onset severe headache followed by rapid loss of consciousness. She had high blood pressure, tachycardia, neck stiffness, and decreased movement on the right side.

If a patient is comatose, calculate the GCS for the summary from the information given (if enough detail on the physical exam is given to calculate this).

The lesion is localized to the CNS (in particular the brain stem reticular activating system or the cerebral cortex diffusely)

Motor pathway left side of brain Meninges and subarachnoid space (with involvement of small arteries and nerves in the meninges)

lesion is localized to pathways left side of brain above the level anywhere above the left midpons and not necessarily to the left motor cortex.

Presence of Doll’s eyes reflexes indicate presence of brain stem functions (and can be used as a measure of severity of brain stem damage). It does not necessarily indicate that the brain stem was intact. The presence of coma suggests involvement of reticular activating systems in the brain stem.

No comment was made in this answer of the likely pathogenesis!

Acute onset in absence of trauma suggests a vascular process especially hemorrhage. However an embolic infarct also may present with a similar time course.

Subarachnoid hemorrhage (ruptured aneurysm/AV malformation)

Cerebellar hemorrhage
Brain stem hemorrhage
Meningitis

Subarachnoid hemorrhage secondary to a ruptured aneurysm (likely congenital berry aneurysm) or AV malformation.

Alternative diagnoses:
Primary intracerebral hemorrhage (cerebellar or brain stem)
acute fulminating meningitis

The suspected hemorrhage is both subarachnoid and intracerebral. This can happen from rupture of eithe ran AVM or aneurysm.

Note a list or classification of alternative diagnoses is asked for. Primary intracerebellar hemorrhage may cause meningismus secondary to herniation or extension of hemorrhage into the subarachnoid space. The word stroke refers to a vascular brain syndrome (secondary to either hemorrhage or infarct) and consequently is not appropriate as an alternative dx. Meningitis is an acceptable alternative diagnosis because it could also cause neck stiffness though the history here is more acute than is likely for this. One would also have to come up with an explanation for the intracerebral involvement (? Abscess, herniation). "Atherosclerotic occlusive disease of cerebral vessels" is better stated as cerebral infarct secondary to thrombotic or embolic disease. Embolic disease could have a sudden onset, cause an intracerebral lesion, should not cause neck stiffness.

Head CT scan: intracranial bleeding/an area of increased "whiteness" owing to the presence of hemoglobin Spinal tap: bloody tap

Hypoperfusion: monitor ICP, EEG and blood flow
Rebleeding of a repaired aneurysm: angiography
Deep coma: continuous monitoring of neurological signs and symptoms
Vasospasm: continuous monitoring of patient with transcranial Doppler ultrasound for signs and symptoms of vasospasm and resulting ischemia within 4-14 days following the SAH.
Hyponatremia: serum electrolyte monitoring
Hydrocephalus: physical exam as well as subsequent cranial ct scans.

Decreased blood supply to brain secondary to vasospasm; loss of cerebral autoregulation; cerebral infarcts secondary to vasospasm. monitor vital signs and ICP. Vasospasm may be detected non invasively with transcranial Doppler recording the flow velocity of the middle cerebral artery.
Recurrent bleeding and intracerebral bleeding e.g. from multiple aneurysms:
angiography ANS disturbances (decreased respiration, cardiac arrhythmia) monitor heart rate, BP and pulse-ox.
Hydrocephalus due to obstruction of CSF flow and absorption secondary to the hemorrhage (CT scan detects hydrocephalus)
Raised intracranial pressure, herniation, damage to brain stem Hyponatremia: serum electrolyte level monitoring
Death

Saccular aneurysms occur at the bifurctions of the arteries at the base of the brain and rupture into the subarachnoid space in the basal cisterns,; 20% of the patients have multiple aneurysms, many at mirror sites bilaterally. The arterial internal elastic lamina disappears at the base of the neck of the aneurysm and the media thins. Connective tissue replaces the smooth muscle cells in the media and the arterial wall is thus more susceptible to small tears. It is not possible to predict which aneurysms are likely to rupture, but most that do average 7 mm in diameter. Early aneurysm repair prevents future hemorrhage and allows for the application of techniques to improve blood flow (e.g. induced hypertension and hypervolemia) should symptomatic vasospasm develop.

Vasospasm leads to delayed ischemia. Nimodipine, a calcium channel blocker, improves outcome in patients with vasospasm. ICP monitoring (with emergency ventriculostomy) is indicated for patients who are lethargic, have neurologic deficits or radiographic evidence of mass effect.

Avoid antihypertensive therapy. You would not want to decrease the blood pressure in this patient even though it is "elevated" because you would decrease perfusion of the brain. You would want to decrease ICP with either hyperventilation and mannitol to promote osmotic diuresis.

The distinction between hemorrhage and meningitis affects treatment. Cause of hemorrhage influences management (aneurysm vs AVM) and prevention of rebleeding.

Vasospasm leading cause of death and disability after aneurysmal rupture. Blood in subarachnoid space is a strong chemical irritant leading to both inflammation of vessel and peroxidation of lipids. Oxyhemoglobin appears to be the stimulant. The occurrence of vasospasm is signficantly related to the amount of blood deposited in the subarachnoid cisterns. Oxyhemoglobin appears to lead to the formation of reactive oxygen species with lipid peroxidation resulting in endothelial injury with impairment of vasodilation and release of endothelin a strong vasoconstrictor. Calcium channel antagonists do not affect the incidence of arteriographic vasospasm and probably improve outcome by other, poorly understood, mechanisms. Optimal treatment awaits the development of agents for blocking or inactivating spasmogenic substances or blocking smooth muscle contraction.

Hemodynamic manipulation: (hypertensive-hypervolemic-hemodilution) Role for keeping blood pressure high with fluids (after aneurysm has been clipped surgically) to maintain cerebral perfusion pressure (CPP = BP-ICP) (cerebral blood flow = CPP/vascular resistance). Note hyperventilation causes hypocapnia with constriction of cerebral arteries with the potential of further reducing cerebral perfusion.

General comments: keep summary brief; ancillary tests, and pathophysiology discussion should focus around the one clinical diagnosis. Pathophysiology needs to be researched e.g. mechanism involved in the vasospasm and the principles underlying maintaining cerebral perfusion despite high ICP.