• Pathophysiology
• Types of Hemorrhagic Stroke
• Causes of Hemorrhagic Stroke
• Symptoms of Hemorrhagic Stroke
• Diagnosis of Hemorrhagic Stroke
• Treatment of Hemorrhagic Stroke
• Rehabilitation & Therapy in Advance Stage
• Home Treatments of Stroke
• Herbal Remedies of Stroke 
• Homeopathic Treatment

Hemorrhagic Stroke is due to bleeding into the brain by the rupture of a blood vessel. Hemorrhagic stroke may be further subdivided into intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). ICH is bleeding into the brain parenchyma, and SAH is bleeding into the subarachnoid space. Hemorrhagic stroke is associated with severe morbidity and high mortality.[2] Progression of hemorrhagic stroke is associated with worse outcomes. Early diagnosis and treatment are important in view of the usual rapid expansion of hemorrhage, causing sudden deterioration of consciousness and neurological dysfunction.

Pathophysiology

The common sites of the bleed are the basal ganglia (50%), cerebral lobes (10% to 20%), the thalamus (15%), pons and the brain stem (10% to 20%), and the cerebellum(10%)(fig.1,2,3). The hematoma disrupts the neurons and glia. This results in oligaemia, neuro-transmitter release, mitochondrial dysfunction, and cellular swelling. Thrombin activates microglia, causes inflammation and edema.[rx][rx]

The primary injury is due to the compression by the hematoma and an increase in the intracranial pressure(ICP).[rx]

Secondary injury is contributed by inflammation, disruption of the blood-brain barrier (BBB), edema, overproduction of free radicals such as reactive oxygen species (ROS), glutamate-induced excitotoxicity, and release of hemoglobin and iron from the clot.

Usually, the hematoma enlarges in 3 hours to 12 hours. The enlargement of hematoma occurs in 3 hours in one-third of cases. The Perihematomal edema increases in 24 hours, peaks around 5–6 days, and lasts up to 14 days. There is an area of hypoperfusion around the hematoma. The factors causing deterioration in ICH are an expansion of hematoma, intraventricular hemorrhage, perihematomal edema, and inflammation.[rx] Cerebellar hematoma produces hydrocephalus by compression of the fourth ventricle in the early stage.

Non-aneurysmal spontaneous subarachnoid hemorrhage may be either perimesencephalic or non-perimesencephalic SAH. In perimesencephalic SAH, bleeding is mainly in the interpeduncular cistern. Physical exertion such as Valsalva maneuver producing increased intrathoracic pressure, and elevated intracranial venous pressure, is a predisposing factor for perimesencephalic nonaneurysmal SAH (PM-SAH).[rx] There is diffuse blood distribution in non-perimesencephalic SAH (NPM-SAH).[rx]

Types of Hemorrhagic Stroke

• Anterior Cerebral Artery (ACA) Infarction – There is significant collateral blood supply in the ACA territory. So, pure ACA strokes are rare. The ACA distribution involves mainly Broca’s area, primary motor, primary sensory and pre-frontal cortex. So patients present with motor aphasia, personality issues, and contralateral leg weakness and numbness. Hand and face are usually spared.
• Middle Cerebral Artery (MCA) Infarction – The MCA has the main trunk (M1) and it divides into two M2 Branches. The M1 (horizontal branch) supplies the basal ganglia and M2 (Sylvian branches) supplies part of the parietal, frontal and temporal lobes. As MCA supplies a wide territory it is extremely important to rule out MCA occlusion. The MCA syndrome causes contralateral arm and facial numbness and weakness, gaze deviation towards the affected side. Aphasia in the left-sided lesions and neglect in the right-sided lesions.
• Posterior Cerebral Artery (PCA) Infarction – The PCA mainly supplies occipital lobe, thalamus and some portion of the temporal lobe. The classic presentation of PCA stroke is homonymous hemianopsia. Apart from this hypersomnolence, cognitive issues, the chemosensory loss can be seen when the deep PCA is involved. Some times there is bilateral infarction of distal PCAs producing cortical blindness and the patient is unaware of the blindness and denies it. This is called Anton-Babinski syndrome.[rx]
• Cerebellar Infarction – The patients with cerebellar strokes present with ataxia, dysarthria, nausea, vomiting, and vertigo.  Lacunar strokes are due to occlusion of small perforating vessels and can be a pure motor, pure sensory and ataxic hemiparetic strokes. In general, these strokes don’t impair memory, cognition, level of consciousness or speech.

Causes of Hemorrhagic Stroke

Hypertension is the most common cause of hemorrhagic stroke.

• Longstanding hypertension produces degeneration of media, breakage of the elastic lamina, and fragmentation of smooth muscles of arteries.
• Lipohyalinosis, fibrinoid necrosis of the subendothelium, microaneurysms, and focal dilatations are seen in the arterioles. The microaneurysms are named as Charcot-Bouchard aneurysms.
• The common sites of origin of hypertension-induced intracerebral hemorrhage are the small penetrating arteries that originate from basilar arteries or the anterior, middle, or posterior cerebral arteries.
• Small artery branches of 50 to 700 μm in diameter often have multiple sites of rupture associated with layers of platelet and fibrin aggregates.
• Hypertensive change causes non-lobar intracranial hemorrhage (ICH). Acute hypertension, as seen in eclampsia, also can cause ICH, known as postpartum ICH.

Cerebral amyloid angiopathy (CAA)

It is an important cause of primary lobar intracerebral hemorrhage in older adults.

• It is characterized by the deposition of the amyloid-β peptide in the capillaries, arterioles, and small- and medium-sized arteries in the cerebral cortex, leptomeninges, and cerebellum.
• This causes ICH in elderly people, commonly associated with variations in the gene encoding apolipoprotein E.
• A familial syndrome can occur in young patients, typically associated with mutations in the gene encoding amyloid precursor protein.
• The incidence of CAA increases with age to the extent that around 50% of those aged more than 70years have CAA. Recurrent hemorrhages can occur due to CAA.

Other Important Causes

• Cigarette smoking and moderate or heavy alcohol consumption and chronic alcoholism.
• Chronic liver disease also increases the chance of ICH due to coagulopathy and thrombocytopenia.
• Decreased low-density lipoprotein cholesterol and low triglycerides are also considered to be risk factors.
• Dual antiplatelet therapy has an increased risk of ICH than monotherapy.
• Sympathomimetics such as cocaine, heroin, amphetamine, ephedrine, and phenylpropanolamine carry an increased risk of a cerebral hemorrhage.
• Cerebral microbleeds (CMBs) associated with hypertension, diabetes mellitus, and cigarette smoking increase the risk of ICH.
• Old age and male sex. The incidence of ICH increases after 55 years of age. The relative risk after 70 years is 7.
• The tumors which are more prone to bleed are glioblastoma, lymphoma, metastasis, meningioma, pituitary adenoma, and hemangioblastoma.

The usual causes of spontaneous subarachnoid hemorrhage (SAH) are ruptured aneurysm of a cerebral artery, arteriovenous malformation, vasculitis, cerebral artery dissection, dural sinus thrombosis, and pituitary apoplexy. The risk factors are hypertension, oral contraceptive pills, substance abuse, and pregnancy.

Intracranial hemorrhage of pregnancy (ICHOP-intracerebral or subarachnoid hemorrhage) occurs with eclampsia. It is due to the loss of cerebrovascular autoregulation.

Symptoms of Hemorrhagic Stroke

The American Stroke Association has suggested the acronym ACT FAST to recognize the early symptoms of a stroke. They include:

• F (Face) – A droop or an uneven smile on a person’s face.
• A (Arms) – Arm numbness or weakness – Elicited by asking the patient to lift the arms
• S (Speech difficulty) – Slurred speech or difficulty in understanding speech
• T (Time) – If any of the above features are present, even if transient, it is time to call the emergency helpline (911).

The additional symptoms of stroke to be watched for are

• Sudden Numbness
• Sudden Confusion
• Sudden Trouble Seeing
• Sudden Trouble Walking
• Sudden Severe Headache

The stroke can be quantified by the NIHSS scale which includes the following

• Visual function
• Level of consciousness
• Sensation and neglect
• Motor function
• Cerebellar function
• Language

A high score suggests proximal vessel occlusion.

Features of middle cerebral artery stroke

• Contralateral hemiparesis and hypesthesia (Weakness of arm& face is worse than in the lower limb)
• Gaze towards to side of lesion
• Ipsilateral hemianopsia
• Receptive or expressive aphasia is dominant hemisphere is affected
• Agnosia
• Inattention, neglect

Features of anterior cerebral artery stroke

• Speech is preserved but there is disinhibition
• Mental status is altered
• Judgment is impaired
• Contralateral cortical sensory deficits
• Contralateral weakness greater in legs than arms
• Urinary incontinence
• Gait apraxia

Posterior cerebral artery stroke

• Cortical blindness
• Contraletarl homonynous heminopsia
• Altered mental status
• Visual agnosia
• Memory impairment

Vertebral/basilar artery stroke

• Nystagmus
• Vertigo
• Diploia and visual field deficits
• Dysarthria
• Dysphagua
• Syncope
• Facial hypersthesia
• Ataxia

Intracerebral hemorrhage

Symptoms almost always occur when the person is awake. Symptoms tend to appear without warning, but they can develop gradually. Symptoms worsen over a period of 30 to 90 minutes. Symptoms can include

• Sudden weakness
• Paralysis or numbness in any part of the body
• Inability to speak
• Inability to control eye movements correctly
• Vomiting
• Difficulty walking
• Irregular breathing
• Stupor
• Coma

Subarachnoid hemorrhage

When caused by a ruptured aneurysm, symptoms can include:

• A very severe headache that starts suddenly (Some people describe it like a “thunderclap.”)
• Loss of consciousness
• Nausea and vomiting
• Inability to look at bright light
• Stiff neck
• Dizziness
• Confusion
• Seizure
• Loss of consciousnes

Diagnosis of Hemorrhagic Stroke

History and Physical

The common presentations of stroke are headache, aphasia, hemiparesis, and facial palsy.[7] The presentation of hemorrhagic stroke is usually acute and progressing. Acute onset headache, vomiting, neck stiffness increases in blood pressure, and the rapidly developing neurological signs are the common clinical manifestations of hemorrhagic stroke.[rx] Symptoms can lead to the extent and location of hemorrhage.

• Headache is more common in a large hematoma.
• Vomiting indicates raised intracranial pressure and is common with cerebellar hematoma.
• Coma occurs in the involvement of the reticular activating system of the brainstem.
• Seizure, aphasia, and hemianopia are seen in lobar hemorrhage. A prodrome consisting of numbness, tingling, and weakness may also occur in lobar bleed.
• Contralateral sensorimotor deficits are the features in hemorrhage of the basal ganglia and thalamus.
• Loss of all sensory modalities is the main feature of thalamic hemorrhage.
• Extension of thalamic hematoma into midbrain can cause vertical gaze palsy, ptosis, and unreactive pupil.
• Cranial nerve dysfunction with contralateral weakness indicates brainstem hematoma.[rx]
• Usually, pontine hematoma produces coma and quadriparesis.[rx]

Cerebellar hemorrhage produces symptoms of raised ICP, such as lethargy, vomiting, bradycardia. Progressive neurological deterioration indicates the enlargement of hematoma or an increase in edema.

The stroke exam is a multi-person coordinated rapid exam.  While staff obtain vitals, attach telemetry, and obtain IV access, the physician performs a rapid neurological evaluation.  National Institutes of Health Stroke Scale (NIHSS) is routinely used to get the baseline evaluation. The exam has to be rapid as “time is brain.”  One must examine the following items:

• The level of consciousness (alert and responsive, arouses to noxious stimuli, comatose…)
• Language (fluency, naming, comprehension, repetition)
• Dysarthria (slurring) which may be picked up in the history
• Motor (subtle arm weakness can be picked up by performing a pronator drift)
• Visual field deficits
• Eye movement abnormalities (in general if a gaze preference is present, the eyes deviate towards the side of the lesion)
• Facial paralysis (asking the patient to smile)
• Ataxia (finger to nose)

With a good history and physical exam, we can localize the stroke. There are various stroke syndromes.

The clinical features of subarachnoid hemorrhage are severe headache described as a thunderclap, vomiting, syncope, photophobia, nuchal rigidity, seizures, and decreased level of consciousness.[rx][rx] Signs of meningismus such as Kernig sign (pain on straightening the knee when the thigh is flexed to 90 degrees) and Brudzinski sign (involuntary hip flexion on flexing the neck of the patient) may be positive.

Imaging

This is followed by a rapid, concise, history and exam such as the NIHSS which is administered simultaneously as the patient gets IV access, telemetry, and labs were drawn.  The patient should then get a stat non-contrasted head computed tomogram (CT) or a combination of head CT, CT Angiography, and perfusion imaging. “Time is brain,” and so we should not waste any time at all.  Ideally, rtPA should be prepared as imaging is occurring, and as soon as the non-contrasted head CT can be visualized, and a bleed is excluded, rtPA should be administered after discussing the risks and benefits, and excluding rtPA contraindications.  Time is critical, as only patients who get all the required studies within 4.5 hours qualify for potentially lifesaving thrombolysis.  After IV rtPA, the CT angiography should be reviewed to determine if the patient qualifies for endovascular therapy as well.

The earliest CT sign of stroke is

• A hyperdense segment of a vessel (direct visualization of the intravascular thrombus/embolus)  – most often seen in the MCA (hyperdense MCA sign and MCA dot sign)

Interpretation of CT perfusion scan

• Infarct core – Demonstrates matched defects in cerebral blood volume (CBV) and mean transit time (MTT)
• Ischemic penumbra – Prolonged MTT, but preserved CBV

Interpretation of magnetic resonance imaging (MRI) scan

• Early hyperacute – Increased diffusion-weighted image (DWI) signal and reduced apparent diffusion coefficient (ADC) values
• Late hyperacute (>6 hours) – High T2 signal in fluid-attenuated inversion recovery (FLAIR) image[rx]

Again in 2018, a significant paradigm shift happened in stroke care. DAWN trial showed significant benefits of endovascular thrombectomy in patients with large vessel occlusion in the arteries of the proximal anterior circulation. This trial extended the stroke window up to 24 hours in selected patients using perfusion imaging. Due to this, we can treat more patients even up to 24 hours.[rx]

All patients should be treated with an antiplatelet agent and a statin, and be admitted for full stroke evaluation. Hypertension is often seen in acute stroke.  This should not be aggressively treated. A baseline electrocardiogram is recommended. The following labs would be indicated when a diagnosis of stroke is entertained:

• Basic metabolic panel (BMP)
• Complete blood count (CBC)
• Cardiac markers
• Coagulation profile: prothrombin time (PT), international normalized ratio (INR), and activated partial thromboplastin time (aPTT)
• Lipid Panel
• Hemoglobin A1C

A transthoracic echocardiogram, telemetry monitoring, and neck vessel imaging are necessary to elucidate the etiology of stroke.

• In the subacute phase – the hematoma may be isodense to brain tissue, and magnetic resonance imaging (MRI) may be necessary. The volume of the hematoma can be measured by the formula AxBxC/2, where A and B are the largest diameter and the diameter perpendicular to that.[rx] C is the vertical height of the hematoma. Intracerebral hemorrhage with a volume of more than 60 cc is associated with high mortality.[rx] The other poor prognostic factors are hematoma expansion, intraventricular hemorrhage, infra-tentorial location, and contrast extravasation on CT scan (spot sign).[3] The paramagnetic properties of deoxyhemoglobin allow early detection of hemorrhage in MRI.[ rx] Gradient echo (GRE) imaging is as good as CT in the detection of acute bleed. MRI can distinguish between the hemorrhagic transformation of infarct and primary hemorrhage. MRI can detect underlying causes of secondary hemorrhages, such as vascular malformations, including cavernomas, tumors, and cerebral vein thrombosis.
• Extravasation of contrast in CT angiogram (CTA) – indicates ongoing bleeding and is associated with fatality.[rx] Multidetector CT angiography(MDCTA) is helpful to rule out the causes of secondary hemorrhagic stroke such as arteriovenous malformation (AVM), ruptured aneurysm, dural venous sinus (or cerebral vein) thrombosis (DVST/CVT), vasculitis, and Moya-Moya disease.[rx] (fig.4).

Certain imaging characteristics help in the differentiation of the underlying disease.[rx]

• Multiple hemorrhages of different ages in parieto-occipital lobes are seen in cerebral amyloid antipathy.
• Hemorrhage in an arterial territory indicates hemorrhagic infarction.
• Multiple stages of bleed in the same hematoma with a fluid level is seen in anticoagulation induced hemorrhage.
• A combination of small ischemic and hemorrhagic lesions indicates vasculitis.
• Hemorrhage in the presence of occlusion of arteries is the feature of Moyamoya disease.

Four- vessel digital subtraction angiography (DSA) – is necessary in the case of SAH. If the DSA is negative for aneurysm, a repeat study is needed to confirm. Repeat angiography is advisable at 1-week and 6-weeks intervals.

Blood investigations – such a bleeding time, clotting time, platelet count, peripheral smear, prothrombin time (PT) and activated partial thromboplastin time(aPTT) will detect any abnormality of bleeding or coagulation and any hematological disorder which can cause hemorrhage.

Liver function tests and renal function tests – are also needed to exclude any hepatic or renal dysfunction as a cause. The investigations to rule out vasculitis are the quantitative evaluation of immunoglobulins, thyroid antibodies, rheumatoid factor, antinuclear antibodies (ANA), anti-double-stranded DNA (ds-DNA antibodies), Histon antibodies, complement, anti-Ro [SS-A] and anti-La [SS-B-] antibodies, cytoplasmic staining and perinuclear staining antineutrophil cytoplasmic antibodies (c- and pANCA), and anti-endothelial antibodies.[rx]

• Electrocardiogram (ECG),
• troponin,
• complete blood count,
• electrolytes,
• blood urea nitrogen (BUN),
• creatinine (Cr), and
• coagulation factors. An
• ECG and troponin are suggested because stroke is often associated with coronary artery disease. A complete blood count can look for anemia or suggest infection.
• Electrolyte abnormalities should be corrected. BUN and Cr should be monitored as contrast studies may worsen kidney function. Coagulation factors, including PTT, PT, and INR, should also be done as the elevated levels can suggest a cause of hemorrhagic stroke.

Treatment of Hemorrhagic Stroke

Emergency treatment with medications.

Therapy with clot-busting drugs must start within 3 hours if they are given into the vein — and the sooner, the better. Quick treatment not only improves your chances of survival but also may reduce complications. You may be given:

• Aspirin – Aspirin is an immediate treatment given in the emergency room to reduce the likelihood of having another stroke. Aspirin prevents blood clots from forming.
• Anticoagulants (eg: heparin) – these medications help to prevent blot clots from getting bigger and prevent new blood clots from forming
• Vinpocetine  – a group of medicine to reached oxygen & nutrition to the hemorrhagic/ischemic area of the brain.
• Vasodilator  – medicine for in ischemic stroke to really reached blood to the obstacle area of the brain.
•  Prednisolone /methylprednisolone –  for the eradication of inflammation in the blood clots area of the brain.
• NSAID –  for inflammation & removing pain.
• Gaba Pentin & Pregabalin –  to recover damage nerve & inhabited the pain impulse to the brain.
• Lipid-lowering agent  – to remove the excessive fat & plaque that are accumulated in the blood vessel in the body.
• Thrombolytic therapy  – these medications dissolve blood clots allowing blood flow to be re-established
• Antihypertensives drug  – in cases of hemorrhagic stroke these medications may be prescribed to help lower high blood pressure
• Antidepressants  – a drug for better sleep & Removed anxiety.
• Muscle Relaxant  – to improved muscle tone & avoid spasticity or bedsore.
• The anti ulcer  – drug used to avoid constipation & normalizing the boil movement.
• Medications of diuretic  – to reduce swelling in the brain and medications to treat underlying causes for the stroke eg: heart rhythm disorders may also be given.
• Intravenous injection of tissue plasminogen activator (TPA) – Some people can benefit from an injection of a recombinant tissue plasminogen activator (TPA), also called alteplase. An injection of TPA is usually given through a vein in the arm. This potent clot-busting drug needs to be given within 4.5 hours after stroke symptoms begin if it’s given in the vein.
• TPA restores blood  – flow by dissolving the blood clot causing your stroke, and it may help people who have had strokes recover more fully. Your doctor will consider certain risks, such as potential bleeding in the brain, to determine if TPA is appropriate for you.

There are many different opinions in the treatment of hemorrhagic stroke. There are many trails on the optimal management of hemorrhagic stroke – Antihypertensive Treatment in Acute Cerebral Hemorrhage(ATACH), Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial ( INTERACT ), Factor VIIa for Acute Hemorrhagic Stroke Treatment (FAST ) and Surgical Trial in Intracerebral Haemorrhage (STICH).[rx] The role of surgery in hemorrhagic stroke is a controversial topic.

• Anticoagulation therapy –  COMPASS trial published in 2017 compared three antiplatelet regimens-  rivaroxaban (2.5 mg twice daily) plus aspirin (100 mg once daily), rivaroxaban (5 mg twice daily), and aspirin (100 mg once daily) in patients with stable atherosclerotic disease (peripheral, coronary, symptomatic carotid artery disease, >50% asymptomatic carotid disease) and found the combination treatment group had a significantly lower risk of major adverse cardiovascular events than with aspirin alone, but a significantly higher risk of major bleeding. Combination treatment is not yet added to guidelines but there is a possibility that this could soon be part of treatment guidelines on secondary prevention of atherosclerotic stroke in select patients. Caution is recommended in patients with a high risk of bleeding.[rx][rx]
• Blood pressure (BP) Management – BP should be reduced gradually to 150/90mmHg, using beta-blockers (labetalol, esmolol), ACE inhibitor (enalapril), calcium channel blocker (nicardipine) or hydralazine. BP should be checked every 10-15 minutes. ATACH study observed a nonsignificant relationship between the magnitude of systolic blood pressure (SBP) reduction and hematoma expansion and 3-month outcome.[rx] But the INTERACT study showed that early intensive BP-lowering treatment attenuated hematoma growth over 72 hours.[rx] It has been found that high SBP is associated with neurological deterioration and death.[rx] The recommendation of the American stroke association (ASA) is that for patients presenting with SBP between 150 and 220 mmHg, the acute lowering of SBP to 140 mmHg is safe and can improve functional outcome. For patients presenting with SBP >220 mmHg, an aggressive reduction of BP with a continuous intravenous infusion is needed.
• Management of Raised Intracranial Pressure (ICP) – The initial treatment for raised ICP is elevating the head of the bed to 30 degrees and osmotic agents (mannitol, hypertonic saline). 20 % mannitol is given at a dose of 1.0 to 1.5 g/kg.[2] Hyperventilation after intubation and sedation, to a pCO of 28 to 32 mmHg will be necessary if ICP increases further. ASA recommends monitoring of ICP with a parenchymal or ventricular catheter for all patients with Glasgow coma scale (GCS) <8 or those with evidence of transtentorial herniation or hydrocephalus.[21] The ventricular catheter has the advantage of drainage of cerebrospinal fluid (CSF) in the case of hydrocephalus. The aim is to keep cerebral perfusion pressure (CPP) between 50 to 70mmHg.
• Hemostatic Therapy – Hemostatic therapy is given to reduce the progression of a hematoma. This is especially important to reverse the coagulopathy in patients taking anticoagulants. Vitamin K, prothrombin complex concentrates (PCCs), recombinant activated factor VII (rFVIIa), fresh frozen plasma (FFP), etc. are used. ASA recommends that patients with thrombocytopenia should receive platelet concentrate. Patients with elevated prothrombin time INR should receive intravenous vitamin K and FFP or PCCs. FFP has the risk of allergic transfusion reactions. PCCs are plasma-derived factor concentrates containing factors II, VII, IX, and X. PCCs can be reconstituted and administered rapidly. The FAST trial showed that rFVIIa reduced the growth of the hematoma but did not improve survival or functional outcome.[rx] rFVIIa is not recommended in unselected patients since it does not replace all clotting factors.
• Antiepileptic Therapy – Around 3 to 17% of patients will have a seizure in the first two weeks, and 30% of patients will show electrical seizure activity on EEG monitoring. Those with clinical seizures or electrographic seizures should be treated with antiepileptic drugs. Lobar hematoma and the enlargement of hematoma produce seizures, which are associated with neurological worsening. Subclinical seizures and non-convulsive status epileptics also can occur. Continuous EEG monitoring is indicated in patients with a decreased level of consciousness. Otherwise, prophylactic anticonvulsant medication is not recommended, according to ASA guidelines.
• Vitamin B therapy – helps in small vessel brain injury (due to a reduction in Homocysteine) but not large artery disease or cardioembolic disease. B-vitamins have a role in primary stroke prevention and are associated with a reduction in primary stroke risk between 7% to 11% in high vascular risk patients (but no reduction in cardiac events is reported). VITATOPS study showed secondary prevention benefits: a reduction in small artery ischemic strokes from 17% to 14% after the intervention, reduction in intracerebral hemorrhage from 18% to 12% after the intervention, reduction in recurrent TIAs from 14% to 10% after intervention and reduction in milder strokes from 22% to 18% after the intervention.[rx]
• Homocysteine-Lowering Therapy – Elevated circulating homocysteine level has been postulated as a risk factor for CVD. However, an updated Cochrane review published in 2017 that included 12 trials (4 new trials since the last review in 2009) found no support for homocysteine-lowering therapy in the form of vitamin B6, B9, or B12 supplements, either alone or in combination, for preventing cardiovascular events (Martí-Carvajal and others 2017

Surgery

Minimally invasive surgery plus recombinant tissue plasminogen activator(rt-PA) for Intracerebral Hemorrhage Evacuation (MISTIE) was a randomized, prospective trial that tested image-guided catheter-based removal of the blood clot.[rx] It showed a reduction in perihematomal edema with clot evacuation.

• The Clot Lysis – Evaluating Accelerated Resolution of IntraVentricularr Hemorrhage (CLEAR IVH) trial showed that low-dose rt-PA can be safely administered to stable intraventricular clots and can increase lysis rates.[rx] Decompressive craniectomy and hematoma evacuation are now being done more frequently for hemorrhagic stroke. Moussa and Khedr showed the improvement in outcome gained by adding decompressive craniectomy with expansive duraplasty to the evacuation of large hypertensive hemispheric ICH in a randomized controlled trial.[rx] Decompressive hemicraniectomy with hematoma evacuation is performed in patients with GCS scores of 8 or less and large hematomas with a volume greater than 60 ml.[rx] It reduces mortality and may improve the functional outcome.

Cerebroprotection

• The secondary injury of hemorrhagic stroke comprises of inflammation, oxidative stress, and toxicity of erythrocyte lysates and thrombin. So, strategies to reduce these are being tried. Pioglitazone, misoprostol, and celecoxib are tried to reduce inflammatory damage. Edaravone, flavanoid, and nicotinamide mononucleotide can reduce oxidative stress. The iron chelator deferoxamine is also in the experimental phase. The safety and neuroprotective efficacy of the cell membrane component citicoline (cytidine-5-phosphocholine) has been shown in some studies.[rx] Rosuvastatin, a competitive inhibitor of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase, was associated with a better outcome in a trial. The calcium channel blocker nimodipine improves outcome in SAH by a neuroprotective effect.[rx]

General Care

• Good medical care, nursing care, and rehabilitation are also of paramount importance. Dysphagia, aspiration, cardiac arrhythmias, stress-induced cardiomyopathy, cardiac failure, acute kidney injury, gastrointestinal bleeding, and urinary tract infection, etc. are common problems. Percutaneous endoscopic gastrostomy (PEG) may be needed to prevent aspiration. Screening for myocardial ischemia with electrocardiogram and cardiac enzyme testing is recommended in hemorrhagic stroke. Intermittent pneumatic compression and elastic stockings reduce the occurrence of deep vein thrombosis. Multidisciplinary rehabilitation is advised to reduce disability.

Rehabilitation

LifeStyle

• Smoking – has been associated with a two to a four-time increased risk of ischemic stroke and intracranial bleeds. It is one of the leading preventable risk factors for stroke. It takes two to four years after smoking cessation for the excess risk to go down.  Smoking cessation options such as counseling, nicotine replacement therapy, or agents such as bupropion should be offered to all appropriate patients. Passive tobacco smoking should be avoided.[rx][rx]
• Regular exercise – (burning 2000 to 3000 calories per week) has been shown to reduce stroke risk by half.[rx]
• Obesity– The risk of ischemic stroke is increased by 22% for overweight individuals and by 64% in obese individuals as compared to normal-weight individuals.[rx]
• Diet– American heart association recommends a diet that has increased intake of fruits, vegetables, and whole grains and limited intake of sugar, saturated fat, trans-fat and red meat. Most Mediterranean diets advocate increased consumption of vegetables, whole grains, fruits, nuts, and olive oil. Moderate amounts of fish, poultry, and dairy products are allowed, whereas red meat is to be avoided. It is uncertain whether the health benefits are due to the consumption of the before mentioned food items, or an under-consumption of red meats (and subsequently decreased intake of saturated fats). Absolute risk reduction is approximately three cardiovascular events per 1000 person-years treated (PREDIMED study).[rx][rx][rx]
• Alcohol– Chronic alcoholism and heavy drinking are risk factors for stroke. J shaped association between alcohol and ischemic stroke risk has been suggested by most studies. There is a protective effect from light to moderate consumption (likely due to an increase in HDL and a decrease in platelet aggregation) and increased risk of stroke with heavy alcohol consumption (due to a hypercoagulable state, alcohol-induced hypertension, cardiomyopathy, and Afib). Stopping or reducing alcohol consumption is recommended for patients with ischemic stroke or TIA.[rx][rx]
• Lower socioeconomic status – including low income, lower education level is associated with an increased risk of stroke recurrence.[rx][rx]

References