Neurological Complications of Hypertension: A Review Article

Neurological Complications Due to Hypertension

As HTN is common in any age group, there are various neurological complications occur in younger and older people with HTN. In children, the incidence of severe arterial hypertension is unknown and it is uncommon [6]. The neurological complications in hypertensive children are facial paresis, acute hemiplegia, and hypertensive encephalopathy. In general, there are 3 clinical syndromes of neurological complications unique to HTN result like hypertensive encephalopathy, lacunar infarction, and hypertensive hemorrhage [7]. So, the importance of measuring BP in adults with neurological symptoms is more widely appreciated than in children, possibly due to a lack of information among pediatricians. Over and above that, neurological complications also occur in a pregnant woman who is suffering from high BP which is known as eclampsia [7].

Stroke Due to Hypertension

Stroke is the highest prevalence neurological complications of HTN. It is a sudden onset of weakness, numbness, paralysis, slurred speech, blurred vision and other features of a sudden interruption in flow of the blood at a specific area of the brain. HTN is the primary pathophysiologic condition in stroke and at the same time it is a modified risk factor. So, it can be reduced by decreasing patient’s high BP. Stoke can be classified into ischemic and hemorrhagic stroke which are contributed by HTN including carotid stenosis, intracranial atherosclerosis, small-vessel arteriosclerosis, and both macroscopic and microscopic aneurysms [8].

HTN can cause stroke through various mechanisms such as high intraluminal pressure will lead to extensive alteration in endothelium and smooth muscle function in intracerebral arteries. The increased stress on the endothelium also can increase permeability over the blood-brain barrier and forms local or multifocal brain edema. Endothelial damage and altered blood cell- endothelium interaction can lead to local thrombi formation and ischemic lesions. In addition, fibrinoid necrosis can cause lacunar infarcts through focal stenosis and occlusions. Degenerative changes in smooth muscle cells and endothelium predisposes for intracerebral hemorrhages [7].

The pathophysiology of stroke which is caused by HTN is due to increase in sympathoadrenal tone with subsequent release of renin and vasoconstriction of arterioles results from direct injury to inhibitory or modulatory brain regions [8]. As a result, it leads to impaired cardiac baroreceptor sensitivity in patients associated with stroke [1]. In ischemic stroke, which is the result of cerebral ischemia, HTN play a compensatory role in maintaining the cerebral perfusion. It has been demonstrated that loss of normal cerebral autoregulation in areas of ischemic brain. Blood flow to the brain becomes directly proportional to mean arterial pressure when autoregulation is lost due to cerebral ischemia. Therefore, it is stated in a theory that pharmacologic increases in BP could have salutatory effects in preserving hypo perfused regions of the brain [1].

Next, the hemorrhagic stroke is caused by HTN associated with cerebral aneurysm formation and subarachnoid hemorrhage where increase in BP causes increase intracranial pressure. As the pressure exceed its limited level, the arteries will rupture at the subarachnoid space which leads to hemorrhage [2].

Hypertensive Encephalopathy Due to Hypertension

The hypertensive encephalopathy is one of the neurological complication consisting of a sudden elevation of arterial pressure usually presented by severe headache and followed by convulsions, coma or a variety of transitory cerebral phenomena. It is also one of several forms of posterior reversible encephalopathy which is also encompassing other causes like renal failure, immunosuppressive therapy and eclampsia [1]. Moreover, hypertensive encephalopathy is a neurologic emergency that can lead to death if untreated. Diagnosis may be delayed when the connection between acute neurologic dysfunction and HTN is not obvious. High BP may be attributed to an underlying neurologic condition or agitation rather than identified as the causative agent [1]. In this headache is a common early complaint, sometimes accompanied by nausea and vomiting. The pathophysiology of hypertensive encephalopathy is due to increased cerebral perfusion from the loss of blood- brain barrier integrity, which results in exudation of fluid into the brain [9]. In normotensive individuals, an increase in systemic blood pressure over a certain range of 60-125 mm Hg induces cerebral arteriolar vasoconstriction, whereby preserving a constant cerebral blood flow and an intact blood-brain barrier. The cerebral autoregulatory range is gradually shifted to higher pressures as an adaptation to the chronic elevation of systemic blood pressure in a chronic hypertensive patient [2].

Hypertensive Retinopathy Due to Hypertension

Hypertensive retinopathy is also one of the neurological complications of HTN where it causes retinal vascular damage. Over a period of time, high BP put its pressure on the optic nerve, causing vision problem by limiting the retinal function. Hypertensive retinopathy classified by mild, moderate and malignant depending on the strength of their associations with systemic vascular disease. Mild is generalized or focal arteriolar narrowing, arteriovenous nicking and increased arteriolar opacity [10]. Whereas moderate means retinal microaneurysm or hemorrhage, cotton wool spot and hard exudates while malignant define as moderate retinopathy and optic disk swelling. On top of that, hypertensive retinopathy is also divided into acute and chronic hypertensive retinal changes. In acute hypertensive retinopathy, optic disc edema is the primary manifestation [11]. The blood supply to the optic nerve arrives via posterior ciliary arteries and peripapillary choroidal vessels. So, the vasoconstriction and choroidal ischemia in the setting of malignant hypertension result in optic disc edema and axoplasmic flow stasis. In chronic hypertensive retinopathy, optic disc pallor develops. Due to the frequent coexistence of HTN and diabetes, diabetic and hypertensive eye complications may also be seen together [10].

Eclampsia in Pregnancy Due to Hypertension

Eclampsia is a severe neuronal complication in pregnant woman where high BP results in seizures. Seizures are periods of disturbed brain activity that can cause episodes of staring, decreased alertness and convulsions during pregnancy. However, the pathogenesis of these complications such as eclamptic seizures, coma, visual disturbances and localizing neurological defects remains poorly understood [12]. Even though the endothelial dysfunction is likely to make a significant contribution but the pathophysiology of underlying eclamptic seizures remain to be elucidated [13].

There are two theories have been proposed based on different hypothesis regarding the cerebrovascular response to systemic hypertension. Firstly, cerebral “overregulation,” leading to vasospasm, ischemia, and intracellular edema. And the next one is the loss of cerebral autoregulation, leading to hyper perfusion, extracellular edema and the posterior reversible encephalopathy syndrome [13].

Treatment and Management for Hypertension Associated with Neurological Complications

HTN contributes to major complications like carotid stenosis, intracranial atherosclerosis, and neuronal effects such as ischemic and hemorrhagic stroke, cerebral aneurysm and so on. But there are certain ways to reduce the rate of mortality caused by HTN associated with neurological complications. For that HTN need to be prevented from each and every individual by Recommendation of lifestyle modification is an initial therapy for patients with BP of 120/80 mmHg or higher. Effective lifestyle includes weight loss, carry out physical activity, reduction in sodium intake, adequate potassium intake, avoid smoking and consuming alcohol and also dietary regimens [4]. Antihypertensive medications are recommended in addition to lifestyle measures for patients with blood pressure of 140/90 mmHg or higher, with a lower threshold of 130/80 mmHg or higher in those with diabetes and chronic kidney disease [14]. For patients without a history of cardiovascular disease or other compelling indication, initiating therapy with a thiazide diuretic such as chlorthalidone is generally recommended. When the BP is 160/100 mmHg or higher, initiating therapy with two-drug combinations is generally recommended [1].

The agents that are recommended by the American Stroke Association (ASA) for acute hypertensive response are either intravenous or transdermal agents with rapid onset and short duration of action to allow precise titration. Table 1 shows the pharmacological characteristics of antihypertensive agents recommended by American Stroke Association [8].

Pharmacological characteristics of antihypertensive agents recommended by American Stroke Association (ASA)

In hypertensive encephalopathy treatment should be given like antihypertensive once structural etiology has been excluded. For patients without a history of hypertension, normal blood pressure parameters are appropriate, but for those with chronic hypertension, an abrupt return to 140/90 mmHg may result in hypoperfusion owing to chronic vascular compensatory changes [1]. Close observation and intravenous antihypertensives are generally indicated. Nitroprusside is a good choice because of its effectiveness, rapid onset, and ease of adjustment [1].

In addition, intravenous dihydropyridine calcium- channel blocking agents and ACE inhibitors are also effective and easy to titrate and may have less-profound effects on cerebral vessels [15]. The underlying cause of the hypertensive episode should be sought. Prognosis in treated patients is generally excellent. Neurologic deficits usually recover completely within 2 weeks. Other than that, medical care for hypertensive retinopathy involves evaluation of secondary causes and appropriate medical management involving lifestyle changes and pharmacotherapy [15].

Treatment that can be given for eclampsia is magnesium sulfate which has been also shown decrease risk in maternal death without evidence of significant harm to the mother or baby [12]. Therefore, intravenous magnesium sulfate should be administered for seizure prophylaxis both during delivery and for 24 hours after delivery. Both phenytoin and diazepam are superior to prevent the recurrence of eclamptic seizures [13]. A range of regimens for magnesium sulphate exists where it is generally administered as a loading dose followed by a continuous infusion for 24 hours postpartum or following the last seizure. Further recurrent seizures can be treated with a further bolus of magnesium sulphate. Seizures which are unresponsive to magnesium sulphate can be treated with benzodiazepines or sodium amobarbital [13].