Introduction

Orthostatic Hypotension (OH) is defined as a decrease in systolic blood pressure of 20 mm Hg, and a decrease in diastolic pressure of over 10 mm Hg on standing or sitting position (₇,₁₃). Frequency of OH in general population is not known accurately. However this rate ranges from 14% to 30% in the group of people over 65 years and increases with age (₁,₁₂,₁₆).

Neurogenic OH is associated with several neurologic diseases such as pandisautonomy, diabetic neuropathy, amyloidosis, hereditary inflammatory polyneuropathies, porphyria, vitamin B12 deficiency, HIV infection, posterior fossa tumors, Parkinson's disease, and multi-system atrophy (₁₀,₁₁,₁₄,₁₅). It has been reported that lesions in central nervous system can cause changes in electrocardiography (₉), cardiac arrythmia (₂,₄), disorders in cardiovascular reflexes (₅) but NOH as a sequel after stroke has been reported in a very limited number of reports (¹¹).

We present a case of isolated neurogenic orthostatic hypotension which occurs as a result of pons infarction extending to mesencephalon due to basilar occlusion.

Case Report

A 58-year-old woman was admitted to hospital with vertigo, blurred vision, and somnolance. The arterial blood pressure of the patient who has been hypertensive for 10 years was 220/110 mm Hg. On neurologic examination she had tendency to sleep, right facial paralysis, extensor response of bilateral plantar reflexes and increased deep tendon reflexes. Cranial computerized tomography was normal and the patient was diagnosed as posterior circulation infarction according to the clinical history and neurological examination and was given heparin. Symptomatic orthostatic hypotension is seen during follow up of the patient. Grade of orthostatic tolerance to tilt-up was 4 (₁₈).There was no orthostatic hypotension in her medical history although chronic anti-hypertensive medication. Systemic arterial tension was found as 140/80 mm Hg on supine position, and 100/60 mm Hg on standing.

While the patient was sitting and standing hypotension was associated with vertigo, and dizziness; and she was able to stand up with support and these symptoms were disappearing totally while she was lying down. She was given sufficient hydration and salt and used elastic socks in addition to anticoagulant therapy. Bilateral large pontin infarction extending to left midbrain (Figure 1 and 2) was detected on cranial magnetic resonance imaging performed at the end of the first week of hospitalization respectively.

Figure 1

Figure 1: T 2 weighted cranial MRI revealed hyperintensities areas in the pons and midbrain

Figure 2

Figure 2: T 2 weighted coronary section of cranial MRI.

In her laboratory examination; complete blood count, fasting blood glucose level, electrolytes, liver-renal-thyroid function tests were totally normal. No pathologic findings were detected in cerebrospinal fluid examination. Serum triglyceride and total cholesterol levels were 245 mg/dl and 426 mg/dl respectively. She was given simvastatin 10 mg/d due to hypercholesterolemia. Electrocardiography, echocardiography, carotid–vertebral artery Doppler examinations and electroneuromyography were normal.

During hospitalization of three weeks and follow up for one year orthostatic hypotension persisted. Grade of tilt-up was 3 in the evaluation of the patients at the end of the first year.

Discussion

Neurogenic OH is pathology in peripheral and central autonomous nervous system that occurs due to insufficient cerebral perfusion when coming into sitting or standing position from supine position. Although OH can be asymptomatic usually causes several symptoms due to decrease of cerebral perfusion. Regulation of systemic blood pressure in different position is maintained by baroreceptor reflexes. These reflexes convey the afferent impulses from aortic arch and carotid sinus to glossopharyngeal and vagal nerve in brain stem and they synapse with nucleus of tractus solitarius. One of the arch of the reflex releases tonic inhibition by decreasing vagal stimulation and causes increasing of the heart rate. The other reflex arch makes peripheral vasoconstriction for the regulation of blood pressure by preventing vasomotor neurons in rostral ventrolateral medulla from inhibition. Third reflex arch increases the blood pressure in long period by stimulating vasopressin release from posterior pituitary gland and increasing body fluid volume. While two reflexes work in seconds the third one works more slowly. Cerebral cortex also plays role by means of hypothalamus in regulation of cardiac and vasomotor activity in addition to basal brain structures (⁵).

It was thought that infarction at the pons extending to the midbrain caused orthostatic hypotension by damaging the connections between medulla oblongata and cerebral cortex through hypothalamus in our case (Figure 3)(₁₇).

Figure 3

Figure 3: Schematic presentation of the afferent connections of the anterior cingulated cortex to important structures in the baroreflex ( NTS: Nucleus Tractus Solitarius, RVLM: Rostral Ventrolateral Medulla, IML: Intermediolateral cell column, PA: Arterial Pressure, NA: Nucleus Ambiguus)

There was not any motor, sensory, and neuro-ophtalmologic sequel in our patient who presented with vertigo, somnolance, and bilateral pyramidal findings. The most important complaints were the symptoms related with OH. Hypotension may develop in lesions of the brain stem due to the effect on afferent autonomous pathways in medulla oblongata De Caro et al demonstrated that there is selective loss of neuron in the dorsal area of solitary tract nuclei in rats with acute heart failure (₃). Even minor lesions in the medulla oblongata especially in acute heart failure may cause autonomic cardiac and respiratory disorders threatening life. There are a lot of case reports about neurogenic OH developed due to posterior fossa tumors (₈,¹⁰,¹⁴,¹⁵). Transient severe OH was described in a case with posterior tegmental pontin infarction in addition to cranial neuropathy and sensorial deficit by Rousseaux et al (¹¹). As a controversy to these studies, no difference in the view of mean arterial blood pressure was observed among the cases with brainstem infarction in a study made by Korpelainen et al (⁵).

As a result, brainstem infarction has to be thought in differential diagnosis of the cases with acute onset OH in whom there is not any peripheral –central pathology as a rare cause.

Correspondence to

Yahya Çelik, MD Trakya University School of Medicine, Neurology Department 22030 Edirne, Turkey Phone : +90-284-2357641/4514 Fax:+90-284-2357652 E mail : celikyahyatr@yahoo.com