A Case of Hypertensive Encephalopathy with Enlarged Optic Nerve Sheath Measured by Transorbital Sonography.

This case report describes our experience in using transorbital sonography to evaluate pathological changes in the central nervous system in hypertensive encephalopathy. A 49-year-old man with nausea, headache, and mild confusion was diagnosed with hypertensive encephalopathy by brain magnetic resonance imaging (MRI), which revealed vasogenic edema in the bilateral thalamus and the brain stem. Lumbar puncture showed no severe intracranial hypertension. Transorbital sonography showed an increase in the optic nerve sheath diameter (ONSD). Repeated examination revealed a return of the ONSD to an almost normal range after a reduction in blood pressure and a resolution of symptoms. An improvement in cerebral vasogenic edema was confirmed by brain MRI. ONSD might be related to the severity of cerebral vasogenic edema. Repeated measurement of ONSD by transorbital sonography may be useful to assess the pathological course and the effect of treatment in hypertensive encephalopathy.

[Efficacy of the energy-modifier cytoflavin in the treatment of patients with hypertensive encephalopathy].

AIM: To evaluate the efficacy of cytoflavin in the treatment of patients with hypertensive encephalopathy (HE). SUBJECTS AND METHODS: One hundred and forty patients aged 39 to 73 years, diagnosed with HE, were examined and randomized to 2 groups. A study group (n = 74) received cytoflavin in a dose of 2 tablets b.i.d. on days 1 to 25 days inclusive during standard basic therapy. A comparison group (n = 66 persons) had standard basic therapy only. A control group consisted of 30 apparently healthy individuals. The investigators studied the frequency of headache, dizziness, and other complaints and the intensity of cephalalgic syndrome, by using a visual analog scale, the quality of life by the Medical Outcomes Study 36-Item Short-Form Health Survey (MOS SF-36) questionnaire, that of sleep by the subjective sleep characteristics questionnaire elaborated at the Moscow City Somnological Center, the level of asthenia by a subjective asthenia rating scale (Multidimensional Fatigue Inventory (MFI-20), and autonomic status, by applying objective and subjective scales on days 1 and 25 of therapy. RESULTS: The study has shown that cytoflavin used in the above dose for 25 days reduces the frequency and magnitude of complaints of headache, dizziness, "venous" complaints, the degree of autonomic and asthenic disorders, and impairments in the quality of sleep and life in the patients with HE at all disease stages. A stepwise discriminant analysis has indicated that the degree of cephalgic syndrome, and autonomic disorders, and worse sleep quality are the most effective points for using the energy-modifier cytoflavin. CONCLUSION: HE treatment based on the current pathogenetic principles may have a preventive impact on the development of HE or slow down the rate of its progression.

Risks of subsequent epilepsy among patients with hypertensive encephalopathy: a nationwide population-based study.

BACKGROUND: To determine whether the diagnosis of hypertensive encephalopathy (HE) is linked to an increased risk of subsequent epilepsy by using a nationwide population-based retrospective study. METHODS: Our study featured a study cohort and a comparison cohort. The study cohort consisted of all patients with newly diagnosed HE between 1997 and 2010, compiled from universal insurance claims data on patients with hypertension taken from the National Health Insurance Research Database. The comparison cohort comprised the remaining hypertensive patients without encephalopathy. The follow-up period was terminated following the development of epilepsy, death, withdrawal from the National Health Insurance system, or the end of 2010. We determined the cumulative incidences and hazard ratios (HRs) of epilepsy development. RESULTS: The incidence of subsequent epilepsy was 2.25-fold higher in the patients with HE than in comparisons (4.17 vs. 1.85 per 1000 person-years), with an adjusted HR of 2.06 (95% CI=1.66-2.56) in the multivariable Cox proportional-hazards regression analysis. The incidence of epilepsy was higher in men, younger patients with HE, and those with brain disorders. CONCLUSIONS: We found that, in Taiwan, patients with HE are at an increased risk of subsequent epilepsy. Physicians should be aware of HE's link to epilepsy when assessing patients with HE.

Hippocampal sclerosis and chronic epilepsy following posterior reversible encephalopathy syndrome.

Chronic epilepsy has rarely been reported after posterior reversible encephalopathy syndrome (PRES) and the association with hippocampal sclerosis has been suggested only once before. We report the case of a girl admitted at the age of 8 years with idiopathic nephrotic syndrome. On the second day of admission, she presented with focal complex seizures and cerebral MRI showed posterior encephalopathy and no hippocampal sclerosis. MRI after one month confirmed the diagnosis of PRES. The seizures recurred and the girl developed pharmacoresistant epilepsy and was admitted to our hospital for further investigation. Cerebral MRI three years after the diagnosis of PRES showed hippocampal sclerosis which was not present on the initial MRI. We conclude that there is a triggering role of PRES in the development of hippocampal sclerosis. Hippocampal sclerosis may have resulted from seizure-associated damage, alternatively, hypertensive encephalopathy may have led to hippocampal damage via a vascular mechanism.

Brainstem swelling and noncommunicating hydrocephalus caused by hypertensive brainstem encephalopathy.

Hypertensive encephalopathy is a life-threatening medical condition manifested by headache, confusion, seizures, and visual disturbance, and, if treatment is delayed, it may progress to coma and death [1, 2] (Chester et al., Neurology 28:928-939, 1978; Vaughan and Delanty, Lancet 356:411-417, 2000). Involvement of the brainstem with or without supratentorial lesions has been reported and is termed hypertensive brainstem encephalopathy (HBE). Cases of HBE involving supratentorial deep gray and white matter are rare and extensive hyperintensity was predominantly seen in brainstem regions on fluid-attenuated inversion recovery and T2-weighted magnetic resonance images. We present radiologic findings of a patient with HBE involving deep supratentorial gray and white matter, causing tonsillar herniation and noncommunicating hydrocephalus by mass effect.

[Cardiorenal syndrome and prerenal azotemia in patients with acute hypertensive encephalopathy].

AIM: To estimate changes in renal function in patients with acute hypertensive encephalopathy (AHE) during standard inpatient antihypertensive therapy. SUBJECTS AND METHODS: Patients were selected for the trial in the cardiology and admission units of a Perm hospital. The group included 60 patients with AHE. The patients received inpatient antihypertensive therapy for 10-14 days. Within the first 2 hours, enalaprilate 1.25 mg was intravenously injected, by monitoring blood pressure. After 6 hours, the patients were given enalaprilate tablets 20 mg b.i.d. plus hydrochlorothiazide 12.5 mg (Subgroup 1) or nifedipine 60 mg plus hydrochlorothiazide 12.5 mg (Subgroup 2). The laboratory parameters of kidney function were measured twice: on admission to and before discharge from hospital. Plasma creatinine and urea concentrations were estimated. Glomerular filtration rate (GFR) and urea/creatinine ratio were calculated. The patients were found to have proteinurea, low GFR, high plasma creatinine concentrations, and increased urea/creatinine ratio. RESULTS: Transient proteinuria was observed in 25% of the patients with AHE within the first 24 hours of the disease. The proportion of patients with lower GFR was unchanged during a 2-week treatment period (20 and 16%, respectively; p = 0.22). There was a rise in the proportion of patients with higher urea/creatinine ratio (83 and 95%, respectively; p = 0.006). CONCLUSION: The course of AHE is complicated by cardiorenal syndrome (CRS) with transient proteinuria and low GFR, as well as by prerenal azotemia (PRA). The number of patients with PRA increased after 2-week conventional inpatient antihypertensive therapy (enalaprilate + hydrochlorothiazide 12.5 mg or nifedipine + hydrochlorothiazide 12.5 mg).

[Neyromidin in the treatment of stage I hypertensive dyscirculatory encephalopathy].

AIM: To evaluate the efficacy and safety of neyromidin in the treatment of Stage I hypertensive dyscirculatory encephalopathy (HDE) and to analyze long-term treatment results. SUBJECTS AND METHODS: Fifty-seven with Stage I dyscirculatory encephalopathy in the presence of grades 1-2 arterial hypertension were examined. Clinical, psychological, and electrophysiological studies were performed and the efficacy of neyromidin was evaluated using the SANDOS geriatric scale. Neyromidin as monotherapy was used as one tablet (20 mg) b.i.d. during a meal. The duration of course treatment was 3 months. RESULTS: Positive changes in the early manifestations of HDE were observed just on day 45 of therapy. The therapeutic effect of the drug manifested as a reduction in the degree of clinical symptoms. There were positive changes in attention, memory, kinetics, verbal associations, counting. The most noticeable improvement was seen in the values of memory and intellectual processes, suggesting higher working capacity, reduced fatigability, and eliminated sluggishness of intellectual processes. EEG displayed a higher amplitude level, a better response to rhythmic photostimulation, and a total power rise in a- and 8-ranges, which was indicative of the activated effect of neyromidin on the functional state of brain structures. CONCLUSION: Neyromidin (20 mg b.i.d. for 3 months) was shown to be effective and well tolerated. The drug reduced the magnitude of clinical manifestations and improved psychological functions and electrophysiological parameters.

[Cognitive functions and extracranial circulation in patients with hypertonic crisis].

We studied effects of enalaprilate and infedipine therapy on the cognitive functions and extracranial circulation in 60 patients with chronic AH complicated by acute encephalopathy. 10% of them had predemential disorders on day 1 of hospitalization and 90% mild cognitive problems. Half of the patients suffered reduced circulation in the common carotid artery. The contribution of impaired extracranial circulation to cognitive dysfunction in the acute period of hypertonic crisis was higher than that of high SAD and DAD. Antihypertensive therapy improved bloodflow in extracranial vessels, decreased their systolic and diastolic indices but failed to eliminate mild cognitive disorders in 65% of the patients. Visual-spatial orientation was restored more frequently than verbal auditory memory. Enalaprilate and infedipine had similar angio- and cerebroprotective effects but the latter had more pronounced favourable effect on verbal auditory memory than the former. The degree of recovery of cognitive function 2 weeks after hypertonic crisis depended not only on the form of cognitive disorder and therapeutic modality but also on the patient's age. Hemodynamic parameters and age 2 weeks after antihypertensive therapy are predictors of residual cognitive dysfunction soon (2 weeks) after recovery.

Manifestations of hypertensive encephalopathy in cats.

OBJECTIVES: Hypertensive encephalopathy in cats is an important entity but is underestimated in clinical practice. This could be explained, in part, by non-specific clinical signs. The objective of this study was to characterise the clinical manifestations of hypertensive encephalopathy in cats. METHODS: Cats with systemic hypertension (SHT) recognised by routine screening, associated with underlying predisposing disease or a clinical presentation suggestive of SHT (neurological or non-neurological), were prospectively enrolled over a 2-year period. Confirmation of SHT was based on at least two sets of measurements of systolic blood pressure >160 mmHg by Doppler sphygmomanometry. RESULTS: Fifty-six hypertensive cats with a median age of 16.5 years were identified; 31 had neurological signs. In 16/31 cats, neurological abnormalities were the primary complaint. The other 15 cats were first presented to the medicine or ophthalmology service, and neurological disease was recognised based on the cat's history. The most common neurological signs were ataxia, various manifestations of seizures and altered behaviour. Individual cats also showed paresis, pleurothotonus, cervical ventroflexion, stupor and facial nerve paralysis. In 28/30 cats, retinal lesions were detected. Of these 28 cats, six presented with a primary complaint of visual deficits, and neurological signs were not the primary complaint; nine presented with non-specific medical issues, without suspicion of SHT-induced organ damage; in 13 cats, neurological issues were the primary complaint and fundic abnormalities were detected subsequently. CONCLUSIONS AND RELEVANCE: SHT is common in older cats and the brain is an important target organ; however, neurological deficits are commonly ignored in cats with SHT. Gait abnormalities, (partial) seizures and even mild behavioural changes should prompt clinicians to consider the presence of SHT. A fundic examination in cats with suspected hypertensive encephalopathy is a sensitive test to support the diagnosis.

Characteristics and Prognosis of Patients With Hypertensive Encephalopathy: A French Nationwide Cohort Study.

BACKGROUND: Hypertensive encephalopathy (HE) constitutes a serious condition, usually observed in patients with long-lasting hypertension. Hypertension-associated HE is sometimes differentiated from the stroke-associated hypertensive emergency. Whether prognosis of hypertension-associated and stroke-associated HE is different is unclear. METHODS: Characteristics and prognosis of HE were assessed in this nationwide retrospective cohort study in all patients with an administrative code of HE compared with age-, sex- and year of inclusion-matched controls admitted to French hospitals during the 2014 to 2022 period. RESULTS: HE was identified in 7769 patients. Chronic kidney disease (19.3%), coronary artery disease (13.8%), diabetes (22.1%), and ischemic stroke (5.2%) were frequent but thrombotic microangiopathy, hemolytic-uremic syndrome, systemic sclerosis or renal infarction were <1%. HE prognosis was poor (death: 10.4%/y, heart failure: 8.6%/y, end-stage kidney disease: 9.0%/y, ischemic stroke: 3.6%/y, hemorrhagic stroke: 1.6%/y, dementia: 4.1%/y). The risk of death was increased to a similar extent in patients with HE, regardless of the presence of known hypertension or concomitant stroke (versus patients without HE). Among patients with HE, known hypertension was significantly associated with increased risks of ischemic stroke, hemorrhagic stroke, heart failure, vascular dementia, and all-cause dementia and to a lesser extent with chronic dialysis in multivariable analyses including adjustment on concomitant stroke. CONCLUSIONS: HE remains a considerable health burden and is associated with a poor prognosis. The distinction between hypertension- versus stroke-associated HE is relevant as these 2 situations convey different risks of stroke, heart failure, vascular dementia, and end-stage kidney disease.

Reversible obstructive hydrocephalus from hypertensive encephalopathy.

BACKGROUND: Diffuse edema involving the posterior fossa may be seen with hypertensive encephalopathy and has rarely been reported to cause hydrocephalus. We present three such cases and review the literature to better delineate this uniquely reversible syndrome. METHODS: Case reports and review of literature. RESULTS: Three patients with hypertensive encephalopathy presented to our institutions with clinical and radiographic features of obstructive hydrocephalus associated with brainstem and cerebellar edema. This required transient external drainage of cerebrospinal fluid (CSF) in two of the three patients. However, with recognition of this unusual syndrome and aggressive management of elevated blood pressure, both edema and hydrocephalus resolved. All patients made complete recoveries and did not require permanent CSF shunting. A review of the literature yielded 15 additional case reports describing reversible obstructive hydrocephalus related to hypertensive encephalopathy. All had mean arterial pressures above 130 mmHg and presented primarily with altered mental status. While half required ventriculostomy, only one required shunting. Excluding a patient who died from sepsis, all recovered neurologically once blood pressure was controlled. CONCLUSION: It is imperative to recognize such cases where hypertension causes edema within the posterior fossa resulting in secondary hydrocephalus. Focusing management on lowering blood pressure avoids unnecessary or prolonged CSF diversion.

Hypertensive encephalopathy presenting as status epilepticus in a three year old.

BACKGROUND: Hypertensive encephalopathy is one of the few neurologic emergencies in which prompt diagnosis and treatment can prevent permanent neurological damage. This syndrome is rarely seen in children. OBJECTIVES: To discuss the recognition of hypertensive encephalopathy as a cause of acute neurological changes in children. CASE REPORT: We present the case of a 3-year-old boy who presented to the Emergency Department with seizures due to hypertensive encephalopathy. A review of the literature on the subject follows the case report. CONCLUSIONS: Hypertensive encephalopathy is a rare cause of acute neurological changes in children that can cause permanent damage if not recognized early. This case illustrates the importance of considering this syndrome as a potential cause of neurological symptoms, especially as neuroimaging can initially be misleading.

Acute cortical blindness in preeclampsia--a case of reversible posterior encephalopathy syndrome.

BACKGROUND: Cortical blindness is one the most disturbing symptoms of reversible posterior encephalopathy syndrome in preeclamptic and eclamptic patients. The disease has been previously associated with a hypertensive breakthrough in the autoregulation of posterior cerebral arterioles followed by extravasation of the fluid into the brain tissue. CASE: 22-year-old primigravida in the 39th week of gestation diagnosed with gestational diabetes mellitus presented with mild preeclampsia and was admitted to our hospital. Antihypertensive treatment was initiated. Her blood pressure remained between 120/80 to 140/90 mm Hg. Glucose levels were within acceptable range. Before the labor induction she developed acute cortical blindness. Magnetic resonance imaging showed vasogenic edema localized in occipital lobes. Cesarean section was performed and anti-edematous treatment initiated. Blindness resolved by the fifth day postpartum. CONCLUSIONS: Reversible posterior encephalopathy developed in our patient in spite of normalized blood pressure that remained within autoregulation limits. Alternative pathogenesis and precipitating factors are discussed.

Primary pigmented nodular adrenal disease presenting as hypertensive crisis.

We present a case of a young girl who presented with hypertensive crisis and recent onset weight gain with hirsutism. On evaluation for Cushing syndrome (CS), her cortisol concentration was high, showed a paradoxical cortisol rise on dexamethasone suppression and the adrenocorticotropic hormone (ACTH) was low. Adrenal imaging showed normal adrenal morphology. Genetic diagnosis of primary pigmented nodular adrenal disease (PPNAD) was made. She was operated for bilateral adrenalectomy and histopathology confirmed the diagnosis of PPNAD. Our case highlights the rare aetiology of PPNAD as a cause of CS resulting in a hypertensive crisis. To the best of our knowledge, this is the youngest case of ACTH independent CS presenting as hypertensive encephalopathy.

Charles Bonnet Syndrome Associated With Recurrent Hypertensive Crisis.

Charles Bonnet syndrome (CBS) is a disorder of visual hallucinations in psychologically normal patients with ocular disease or damage to visual pathways. The etiology of CBS is not fully understood. It is associated with various triggers, with age-related macular degeneration the most common; other triggers are systemic diseases such as stroke, multiple sclerosis, and anemia as well as lighting issues, fatigue, and medical or surgical eye treatments. Visual disturbances such as decreased visual acuity, visual field deficits, or visual hallucinations are common in association with hypertensive encephalopathy. We describe a patient with episodic CBS triggered by recurrent hypertensive crises, which resolved with blood pressure management in the hospital setting.

Homozygous familial hypercholesterolaemia in a patient presenting with hypertensive encephalopathy.

Homozygous familial hypercholesterolaemia (HoFH) is a disorder affecting low-density lipoprotein (LDL) receptor genes. Patients typically have a triad of elevated LDL-cholesterol (LDL-C), xanthomatosis and premature atherosclerotic cardiovascular disease. Our patient, a preteen boy, presented with signs of hypertensive encephalopathy. Physical examination showed arcus cornealis, planar xanthomas and tuberous xanthomas. After appropriate investigations, a direct aetiology of the hypertension could not be elucidated; however, our patient's hypertension resolved with the reduction in serum lipid levels. ß-hydroxy ß-methylglutaryl coenzyme A reductase and cholesterol absorption inhibitors were administered as first-line treatment. A significant proportion of patients with HoFH continue to have elevated LDL-C levels, thereby requiring second-line agents, such as proprotein convertase subtilisin/kexin type inhibitors (evolocumab), microsomal triglyceride transfer protein inhibitors (lomitapide) and angiopoietin-like protein inhibitors (evinacumab). This case report aimed to raise awareness among paediatricians to consider HoFH as a possible aetiology in a child presenting with hypertension and suggestive physical findings.

A case of reversible posterior leukoencephalopathy syndrome with acute hypotension.

Reversible posterior leukoencephalopathy syndrome (RPLS) is theoretically associated with hypertensive encephalopathy because the most patients demonstrate abrupt increasing of blood pressure (BP). A 59-year-old woman, who had undergone cholecystectomy 4 days before, complained of a headache and rapidly progressing visual disturbance. Her BP was postoperatively controlled at around 150/80, but her BP was 89/46 when she noticed her symptoms. Magnetic resonance imaging showed vasogenic edema in bilateral occipital and right parietal lobes, and intracranial magnetic resonance angiography revealed bilateral diffuse peripheral vasoconstriction. After discontinuing ropivacaine administration via epidural catheter, her BP rose to 114/62 and her symptoms completely disappeared within a few days. Except for hypotension, the clinical course and the radiological evidences in our case were consistent with RPLE. This case supports another hypothesis of RPLS mechanism that arterial endothelial injury by toxic drug effect results in transudation of fluid from blood vessels causing vasogenic brain edema.

Reversible posterior leukoencephalopathy syndrome in a patient with severe uremic encephalopathy.

A 59-year-old male presented at our hospital with disturbance of consciousness. He had severe neurological disturbances associated with uremia caused by severe renal insufficiency. Cranial computed tomography (CT) was normal on admission. FLAIR-weighted MRI showed increased signal intensities bilaterally in the cortical and subcortical areas of the occipital lobe. Repeated hemodialysis resulted in improvement of the clinical symptoms and blood chemistry, and normalization of the MRI findings. Although the patient was discharged without neurological deficit, he had to be maintained on regular intermittent hemodialysis due to persistent renal failure. These reversible neuroradiological abnormalities may have been caused by reversible brain edema, but other pathoetiological factors should be also considered, such as abnormalities of cerebral metabolism and effects of uremic toxins.

Posterior reversible encephalopathy syndrome in an 87-year-old woman with Escherichia coli bloodstream infection.

We present the case of an 87-year-old woman with history of hypertension, hypercholesterolemia, ischemic heart diseases, urinary tract infections, and cerebrovascular disease who experienced a transient clinical picture characterized by confusion, lethargy, and acute renal dysfunction in the course of urinary tract infection with Escherichia coli bacteremia. Escherichia coli bloodstream infection was associated with brain computed tomography (CT) and magnetic resonance imaging (MRI) patterns in which the lesion distribution was consistent with posterior reversible encephalopathy syndrome (PRES). Diagnosis of PRES was confirmed by demonstration of vasogenic edema on apparent diffusion coefficient (ADC) maps and near-complete resolution of clinical manifestations at discharge.

Posterior reversible encephalopathy syndrome in a patient with hepatitis B induced type 1 membranoproliferative glomerulonephritis.

Posterior reversible encephalopathy syndrome (PRES) is a rare complication of nephrotic syndrome and corticosteroid therapy. Here, we discuss an 18 year old man with type 1 membranoproliferative glomerulonephritis (MPGN) secondary to hepatitis B infection who developed posterior leukoencephalopathy while on therapy with lamivudine and prednisone. He developed seizures and vision loss. He also had hypertension, but no sudden elevation was recorded at any time. Magnetic resonance imaging revealed patchy areas of altered signal intensity involving cortical gray and subcortical white matter in the bilateral frontoparietal regions, occipital cortices, temporal cortices and cerebellar hemispheres, and hyperintensity on T2W and FLAIR sequences. Tapering of prednisone and controlling hypertension resulted in clinical improvement within a few days, and in a month MRI was normal. Diagnosing PRES requires a high index of suspicion when treating similarly susceptible patients. PRES as a complication during the treatment of MPGN secondary to hepatitis B has, to our knowledge, never been reported previously in the literature.