IPHREHAB : Intracranial Hemorrhage

IPHREHAB

Intracranial Hemorrhage
This is the common, well-known “spontaneous” brain hemorrhage. It is due predominantly to chronic hypertension and degenerative changes in cerebral arteries.Hemorrhage may interfere with cerebral function through a variety of mechanisms, including destruction or compression of brain tissue and compression of vascular structures, leading to secondary ischaemia and edema.
Intracranial hemorrhage is classified by its location as intracerebral, subarachnoid, subdural, or epidural, all of which- except subdural hemorrhage- are usually  caused by arterial bleeding.


The bleeding occurs within brain tissue, and rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms. The extravasation forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues . Adjacent brain tissue is distorted and compressed. If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers are compromised, leading to coma and death.

1. Intracerebral Hemorrhage

Of all the cerebrovascular diseases, brain hemorrhage is the most dramatic.It has been given its own name, “apoplexy”.

Clinical Picture

• With smaller hemorrhages, the clinical picture conforms more closely to the usual temporal profile of a stroke, i.e, an abrupt onset of symptoms that evolve gradually and steadily over minutes, hours, or a day or two, depending on the size of the ruptured artery and the speed of bleeding. 
• Headache and vomiting are cardinal features.Very small hemorrhages in “silent” regions of the brain may escape clinical detection.
• Clinical features vary with the site of hemorrhage.
• Deep cerebral hemorrhage  The two most common sites of hypertensive hemorrhage are the putamen and the thalamus, which are separated by the posterior limb of the internal capsule. This segment of the internal capsule is traversed by descending motor fibers and ascending sensory fibers, including the optic radiations.
• Lobar hemorrhage  Hypertensive hemorrhages also occur in subcortical white matter underlying the frontal, parietal, temporal, and occipital lobes. Symptoms and signs vary according to the location.
• Pontine hemorrhage  With bleeding into the pons, coma occurs within seconds to minutes and usually leads to death within 48 hours. Ocular findings typically include pinpoint pupils. Horizontal eye movements are absent or impaired, but vertical eye movements may be preserved.
• Cerebellar hemorrhage  The distinctive symptoms of cerebellar hemorrhage (headache, dizziness, vomiting, and the inability to stand or walk) begin suddenly, within minutes after onset of bleeding.

Laboratory Findings  

Among laboratory methods for the diagnosis of intracerebral hemorrhage, the CT scan occupies the foremost position. In CT scans, fresh blood is visualized as a white mass as soon as it is shed. The mass effect and the surrounding extruded serum and edema are hypodense.

By MRI, either in T1-or-T2 weighted images, the hemorrhage is not easily visible in the 2 or 3 days after bleeding.

In general, lumbar puncture is ill advised, for it may precipitate or aggravate an impending shift of central structures and herniation. The white cell count in the peripheral blood may rise transiently to 15,000 per cubic millimeter, a higher figure than in thrombosis.

Differential Diagnosis: 

Putaminal, thalamic, and lobar hypertensive hemorrhages may be difficult to distinguish from cerebral infarctions. To some extent, the presence of severe headache, nausea and vomiting, and impairment of consciousness are useful clues that a hemorrhage may have occurred; the CT scan  identifies the underlying disorder definitively.

CT scan or MRI is the most useful diagnostic procedure, since hematomas can be quickly and accurately localized.

IPHREHAB : DIFFERENTIAL DIAGNOSIS AND TREATMENT CEREBRAL THROMBOSIS AND TIAs

IPHREHAB

DIFFERENTIAL DIAGNOSIS CEREBRAL THROMBOSIS AND TIA


Differential Diagnosis
Vascular disorders are mistaken for ischaemic stroke include intracerebral hemorrhage, subdural or epidural hematoma , and subarachnoid hemorrhage from rupture of an aneurysm or vascular malformation. These condition can often be distinguished by a history of trauma or of excruciating headache at onset, a more marked depression of consciousness, or by the presence of neck stiffness on examination. They can be excluded  by CT scan or MRI.


Differential Diagnosis: Other structural brain lesion such as tumor or abscess can also produce focal cerebral symptoms of acute onset. Brain abscess is suggested by concurrent fever, and both abscess and tumor can usually be diagnosed by CT scan or MRI. Metabolic disturbances, particularly hypoglycemia and hyperosmolar nonketotic hyperglycemia, may present in stroke like fashion. The serum glucose level should therefore be determined in all patients with apparent stroke.

Treatment of Cerebral Thrombosis and Transient Ischemic Attacks

The current treatment of it may be divided into four parts:

Management in the acute phase

Measures to restore the circulation and arrest the pathologic process

    1. Thrombolytic agents ( t-PA only for completed stroke,w/in 3~6hrs ) 2.Anticoagulant drugs ( Heparin, LMWH & warfarin)

    3. Antiplatelet drugs ( Aspirin  or  Clopidogrel, Dipyridamole or   Ticlopidine )

    4.Difibrase

    5. Neuroprotective agents: barbiturates, opioid  antagonist naloxone,Manitol

Treatment

Treatment of cerebral edema and raised intracranial pressure

Acute surgical revascularization 

Surgery for symptomatic carotid stenosis, Carotid endarterectomy, intralumenal stents, extracranial-intracranial bypass

Physical therapy and rehabilitation.

Measures to prevent further strokes and progression of vascular disease.

• Since the primary objective in the treatment  of  atherothrombotic disease is prevention , efforts to control the risk factors must continue. 
• Aspirin
• Hypotensive agents
• Oversedation should be avoided
• Systemic hypotension, severe anemia should be treated promptly
• Particular care should be taken to maintain the systemic blood pressure, oxygenation  and intracranial  blood flow during surgical procedures, especially in elderly patient.

Course and Prognosis

When the patient is seen early in the cerebral thrombosis, it is difficult to give an accurate prognosis.

As for the eventual or long-term prognosis of the neurologic deficit , there are many possibilities.

It must be mentioned that having had one thrombotic stroke, the patient is at risk in the ensuing months and years of having a stroke at the same or another site, especially if there is hypertension or diabetes mellitus.

IPHREHAB : Transient Ischemic Attacks(TIA) & CEREBRAL THROMBOSIS

IPHREHAB

1.Transient Ischemic Attacks(TIA)
Current opinion holds that TIAs are brief, reversible episodes of focal, nonconvulsive ischaemic neurologic disturbance, Consensus has been that their duration should be less than 24 h.

Clinical picture
Transient Ischaemic Attacks can reflect the involvement of any cerebral artery. The loss of function entirely depends on the influenced artery. It may last  a  few seconds or up to 12 to 24 h, Most of them last 2 to 15 min. There are only a few attacks or several hundred. Between attacks, the neurologic examination may disclose no abnormalities. A stroke may occur after numerous attacks have occurred over a period of weeks or months.

Differential diagnosis of TIAs

Transient episodes, indistinguishable from TIAs, are known to occur in patients with Seizure,Migraine,Transient global amnesia,and occasionally in patients with multiple sclerosis, meningioma, glioblastoma ,metastatic brain tumors situated in or near the cortex ,and even with subdural hematoma.

2. Cerebral thrombosis

Most cerebrovascular disease can be attributed to atheroscleroses and chronic hypertension; until ways are found to prevent or control them, vascular disease of the brain will continue to be a major cause of morbidity.

Pathogenesis

Pathogenesis of Ischemic neuronal death

   Ischemia

       ↓ 

   Excitatory amino acid receptors

       ↓ 

   Borderzone or penumbra    ↓

   Programmed cell death

Clinical picture  

In general, evolution of the clinical phenomena in relation to cerebral thrombosis is more variable than that of embolism and hemorrhage. The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischaemic process.

Clinical picture

In more than half of  patients, the main part of the stroke is preceded by minor signs or one or more transient attacks of focal neurologic dysfunction. The final stroke may be preceded by one or two attacks or a hundred or more brief TIAs, and stroke may follow the onset of the attacks by hours, weeks, or, rarely, months.

The most occurrence of the thrombotic stroke is during sleep.The patient awakens paralyzed. Either during the night or in the morning.

Unaware of any difficulty, he may arise and fall helplessly to the floor with the first step.

Clinical picture

Associated symptoms

Seizures accompany the onset of stroke in a small number of cases (10-50%); in other instances, they follow the stroke by weeks to years. The presence of seizures does not definitively distinguish embolic from thrombotic strokes, but seizure at the onset of  stroke may be more common with embolus.

Headache  occurs in about 25% of patients with ischaemic stroke, possibly because of the acute dilation of collateral vessels.

Laboratory Findings

• CT Scan or MRI: A CT scan or MRI  should be obtained routinely to distinguish between infarction and hemorrhage as the cause of stroke, to exclude other lesions (eg, tumor, abscess) that can mimic stroke, and to localize the lesion. CT is usually preferred for initial diagnosis because it is widely available and rapid and can readily make the critical distinction between ischaemia and hemorrhage.
• Lumbar Puncture: This should be performed in selected cases to exclude subarachnoid hemorrhage.
• Cerebral Angiography: Intra-arterial angiography is used to identify operable extracranial carotid lesions in patients with anterior circulation TIAs who are good surgical candidates. It also can be used for intra-arterial thrombolysis ( r-tPA)
• Magnetic resonance  Angiography (MRA) may detect stenosis of large cerebral arteries, aneurysms, and other vascular lesion, but its sensitivity is generally inferior to that of conventional angiography.

IPHREHAB : CEREBRAL ISCHEMIA AND INFARCTION

IPHREHAB :

 CEREBRAL ISCHEMIA AND INFARCTION


Cerebral ischaemia and infarction
Anatomy and pathology
The principal pathological process under consideration here is the occlusion of arteries supplying the brain. The two internal carotid arteries and the basilar artery form the Circle of Willis at the base of the brain, which acts as an efficient anatomotic device in the event of occlusion of arteries proximal to it.

CIRCLE OF WILLIS

Anatomy and pathology

VERTEBRAL ARTERY

Occlusion leads to sudden severe ischaemia in the area of brain tissue supplied by the occluded artery, and recovery depends upon rapid lysis or fragmentation of the occluding material: Reversal of neurological function within minutes or hours gives rise  to the clinical picture of a transient ischaemic attack.

When the neurological deficit lasts longer than 24 hours, it may be called a reversible ischaemic neurological deficit ( RIND ) if it recovers completely in a few days, or a completed stroke if there is a persistent deficit. Sometimes recovery is very slow and incomplete.

Neurological symptoms and signs  

The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischaemic process.      

 Neurological symptoms and signs

BASIC

The following suggest middle cerebral territory:

Dysphasia; Dyslexia, dysgraphia, dyscalculia; Loss of use of contralateral face and arm; Loss of feeling in contralateral face and arm.

• The following suggests anterior cerebral territory:

Loss of use and/ or feeling in the contralateral leg.

• The following suggests posterior cerebral territory:

Development of a contralateral homonymous hemianopia.

Neurological symptoms and signs

The following suggests a deep-seated lesion affecting the internal capsule which is supplied by small perforating branches of the middle and posterior cerebral arteries close to their origins: Complete loss of motor and sensory function throughout the whole of the contralateral side of the body with a homonymous hemianopia.

Neurological symptoms and signs

The following suggests ophthalmic artery territory (the ophthalmic artery arises from the internal carotid artery just below the Circle of Willis): Monocular loss of vision.

Neurological symptoms and signs

The following suggest vertebro-basilar territory: double vision( 3,4,6);

facial numbness(5);

facial weakness(7);

vertigo (8);

dysphagia (9, 10);

dysarthria ( 9, 10, 12);

ataxia; drop attacks;

motor or sensory loss in both arms or legs.

IPHREHAB : Cerebral Vascular Disease & Stroke

IPHREHAB


Cerebral vascular Disease
Definition of term:
The term cerebrovascular disease designates any abnormality of the brain resulting from a pathologic process of the blood vessels. Sudden loss of neurological function is the hallmark of cerebrovascular disease.
Cerebrovascular disease is the third most common cause of death and the most common disabling neurologic disorder in western civilized countries where an increasing proportion of people survive to old age.
Its incidence increases with age and is somewhat higher in men than in women.


Risk factors for stroke
Systolic or diastolic hypertension

Diabetics
Hypercholesterolemia
Heart disease (afib)
Cigarette smoking
Heavy alcohol consumption
High homocystine
Oral contraceptive use

The major types of cerebrovascular disease

Cerebral ischaemia and infarction

Transient Ischemic Attacks

Atherosclerotic thrombosis

Lacunes

Embolism

Hemorrhage

Hypertensive hemorrhage

Ruptured aneurysms and vascular malformations

Other