Neuropathology of Spontaneous Hypertensive Encephalopathy in Cats.

Pathologic features of 12 cats with naturally acquired systemic hypertension and concomitant hypertensive encephalopathy were analyzed. All cats demonstrated acute onset of signs localized to the forebrain and/or brainstem, including stupor, coma, and seizures. All cats had systemic hypertension, ranging from 160 to 300 mm Hg. Gross lesions were identified in 4 of 12 cases, including caudal herniation of the cerebrum and cerebellum, sometimes with compression of the rostral colliculus and medulla. Histologically, all cases featured bilaterally symmetrical edema of the cerebral white matter. Associated vascular lesions, especially arteriolar hyalinosis, were also observed. Concurrent lesions were chronic tubulointerstitial nephritis (11/12 cases), adenomatous hyperplasia of the thyroid gland (4 cases), hypertensive choroidal arteriopathy (6 cases), and left ventricular hypertrophy (5 cases). This study demonstrates that the typical histologic manifestation of spontaneous hypertensive encephalopathy in cats is bilaterally symmetrical edema of the subcortical cerebral white matter.

Hypertensive encephalopathy mimicking cerebral vasculitis with pontine oedema, cerebellar white matter lesions and multiple cerebral infarctions.

A 47-year-old man with poorly controlled hypertension presented with headaches, right-sided weakness and dysarthria. CT and MRI scans of the brain showed widespread abnormalities including significant pontine oedema, basal ganglia and corona radiata infarctions and cerebellar white matter high signal. Imaging of the intracerebral vasculature also demonstrated wall irregularities. Initially a central nervous system inflammatory disorder was thought to be the most likely diagnosis, possibly acute demyelinating encephalomyelitis or cerebral vasculitis, and the patient was treated with high-dose intravenous steroids. The diagnosis of hypertensive encephalopathy was made because (1) the patient was hypertensive and (2) the patients MRI findings resolved with antihypertensive treatment.Blood pressure treatment was instigated from admission, and the patients symptoms improved with resolution of the radiological abnormalities.

[THE EFFECTIVENESS OF DIAGNOSIS AND TREATMENT OF CEREBROVASCULAR DISORDERS IN HYPERTENSIVE ENCEPHALOPATHY IN ELDERLY PATIENTS BY STUDYING THE CHARACTERISTICS OF CEREBRAL HEMODYNAMICS AND CEREBRAL PERFUSION STATUS].

Intrigue progression of hypertensive encephalopathy (HE) in older patients is that the development of cognitive impairment and high blood pressure underestimated, aslo exist without clinical manifestations. In recent decades convincing proved that the basis for the development of various diseases is cerebral dysfunction systems regulating brain blood flow, including--autoregulation system, which largely affects the blood supply to the brain. This explains the fact that patients with chronic brain ischemia cerebral hemodynamic status largely depends on the condition and stability of the regulatory mechanisms of systemic and cerebral hemodynamics, particularly of systemic blood pressure, regional cerebral blood supply, normalization which, in the early stages of development disorders, prevents of serious complications. In this paper the theoretical generalization and new solution of scientific and practical problems of hypertension influence on the formation of chronic cerebral ischemia in elderly patients on a background of hypertension--specified risk factors and especially the formation of a comprehensive study on the basis of clinical and neurological data, tool sand methods for neuroimaging research developed and improved methods of diagnosis. Found that in elderly patients with HE and HBP observed significant (P < 0.05) increase in the thickness of the intima-media complex was significantly higher (dextra--1.12 ± 0.03 and sinistra--1.11 ± 0.03), than middle-aged patients with hypertension at HE, which constitutes a violation of the elastic properties of the vascular wall. Established correlation data radionuclide study ultrasonic duplex scanning of vessels of the head and neck. A negative correlation of intima-media and severity of lesions according to hypoperfusion of computer tomography single photon emission (r = -0.49; P < 0.05); confirming the progression of HE in elderly patients needs improvement and treatment.

[Cytoflavin® effect on endothelium function and cerebral hemodynamics in patients with hypertensive enceplalopathy].

One hundred forty patients (the average age of 46.7 ± 7.7 years) with hypertensive encephalopathy (HE) were observed. 74 patients of the main group received Cytoflavin in a dose of 2 tablets twise a day in the standard basic therapy. 66 patients of the reference group received the basic therapy alone. The arterial endothelium function was estimated and ultrasonic examination of the hemodynamics at five structurally functional levels of the cerebral vascular course was used. All the patients with HE had endothelial dysfunction, bloodstream depression in the arterial course of the brain vascular system, decreased reactivity of the intracranial veins, difficulty in venous outflow. In the course of the therapy with Cytoflavin restotation of the arterial endothelial function in the patients with HE I stage, the linear and volume speed of bloodstream in the main and intracranial cerebral arteries in the patients with HE I-II stages, restoration of the intracranial veins reactivity, the linear speed of bloodstream in intracranial veins in the patients with all three stages of HE, the linear speed of bloodstream in the main veins up to the control values in the patients with I-III stages of HE were observed. Interrelation between the values of the cerebral hemodynamics and the state of the endothelium function was shown.

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.

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.

Neuroprotection and sex steroid hormones: evidence of estradiol-mediated protection in hypertensive encephalopathy.

Besides their effects on reproduction, estrogens exert neuroprotective effects for brain diseases. Thus, estrogens ameliorate the negative aspects of aging and age-associated diseases in the nervous system, including hypertension. Within the brain, the hippocampus is sensitive to the effects of hypertension, as exemplified in a genetic model, the spontaneously hypertensive rat (SHR). In the dentate gyrus of the hippocampus, SHR present decreased neurogenesis, astrogliosis, low expression of brain derived neurotrophic factor (BDNF), decreased number of neurons in the hilus and increased basal levels of the estrogen-synthesizing enzyme aromatase, with respect to the Wistar Kyoto (WKY) normotensive strain. In the hypothalamus, SHR show increased expression of the hypertensinogenic peptide arginine vasopressin (AVP) and its V1b receptor. From the therapeutic point of view, it was highly rewarding that estradiol treatment decreased blood pressure and attenuated brain abnormalities of SHR, rendering hypertension a suitable model to test estrogen neuroprotection. When estradiol treatment was given for 2 weeks, SHR normalized their faulty brain parameters. This was shown by the enhancement of neurogenesis in the dentate gyrus, according to increased bromodeoxyuridine incorporation and doublecortin labeling, decreased reactive astrogliosis, increased BDNF mRNA and protein expression in the dentate gyrus, increased neuronal number in the hilus of the dentate gyrus and a further hyperexpression of aromatase. The presence of estradiol receptors in hippocampus and hypothalamus suggests the possibility of direct effects of estradiol on brain cells. Successful neuroprotection produced by estradiol in hypertensive rats should encourage the treatment with non-feminizing estrogens and estrogen receptor modulators for age-associated diseases.

Posterior reversible encephalopathy syndrome in childhood: report of four cases and review of the literature.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) is a recently described disorder with typical radiological findings of bilateral gray and white matter abnormalities in the posterior regions of the cerebral hemispheres and cerebellum. Its clinical symptoms include headache, decreased alertness, mental abnormalities such as confusion, diminished spontaneity of speech, and changed behavior ranging from drowsiness to stupor, seizures, vomiting, and abnormalities of visual perception such as cortical blindness. In this study, the clinical and radiological findings of 4 children with this syndrome due to a variety of conditions are reported. METHODS: The records of 4 children with a diagnosis of PRES were retrospectively analyzed. RESULTS: PRES is associated with a disorder of cerebrovascular autoregulation of multiple etiologies. Four patients with PRES who had primary diagnoses of severe aplastic anemia, nephritic syndrome, Henoch-Schönlein purpura, and acute poststreptococcal glomerulonephritis are presented. This syndrome has been described in numerous medical conditions, including hypertensive encephalopathy, eclampsia, and with the use of immunosuppressive drugs. CONCLUSIONS: Early recognition of PRES as a complication during different diseases and therapies in childhood may facilitate precise diagnosis and appropriate treatment.

Hypertensive crisis in young woman with Takayasu arteritis.

A young woman who was experiencing repeated convulsions was admitted. The patient's brain magnetic resonance image revealed reversible posterior leukoencephalopathy. Blood pressure fluctuated at times to more than 200 mmHg, and the measurement of the right and left upper arms differed by approximately 70 mmHg. Enhanced computed tomography revealed stenotic lesions of some arteries including the left renal artery. Such findings led to an initial diagnosis of Takayasu arteritis and hypertensive encephalopathy caused by renovascular hypertension. A percutaneous transluminal renal angioplasty was successfully performed. The patient's blood pressure returned to normal value without the use of antihypertensive drugs.

Reversible brainstem edema due to hypertensive encephalopathy in an 8-year-old girl.

The authors report an 8-year-old girl with refractory status epilepticus due to hypertensive encephalopathy, secondary to end-stage renal disease. Brain magnetic resonance imaging (MRI) in the acute phase showed striking hyperintensities in the brain stem and medial thalamus along with subtle cortical lesions. After successful control of hypertensive crisis and status epilepticus, the patient recovered to her baseline. Near total resolution of the lesions was noted on follow-up imaging performed 9 days later. Predominant brainstem involvement as a feature of posterior reversible encephalopathy syndrome due to hypertensive crisis is extremely rare in children and has not been well documented.

Posterior reversible encephalopathy syndrome (PRES) with immune system activation, VEGF up-regulation, and cerebral amyloid angiopathy.

The case of a 75-year-old man with a history of lymphoma, recent upper respiratory tract infection, and a protracted course of encephalopathy is presented. Radiologically, findings were consistent with posterior reversible encephalopathy syndrome. A brain biopsy revealed evidence of endothelial activation, T-cell trafficking, and vascular endothelial growth factor expression, suggesting that systemic immune system activation may be involved with triggering posterior reversible encephalopathy syndrome. In addition, underlying cerebral amyloid angiopathy may have contributed to the initial nonclassical edema distribution by compromising autoregulatory blood flow mechanisms.

Posterior reversible encephalopathy syndrome during posterior fossa tumor resection in a child.

Posterior reversible encephalopathy syndrome (PRES) has been described in the setting of malignant hypertension, renal disease, eclampsia, and immunosuppression. In addition, a single case of intraoperative (posterior fossa craniotomy) PRES has been reported; however, this case occurred in an adult. The authors present a clinically and radiographically documented case of intraoperative PRES complicating the resection of a posterior fossa tumor in a 6-year-old child. During tumor resection, untoward force was used to circumferentially dissect the tumor, and excessive manipulation of the brainstem led to severe hypertension for a 10-minute period. An immediate postoperative MR image was obtained to rule out residual tumor, but instead the image showed findings consistent with PRES. Moreover, the patient's postoperative clinical findings were consistent with PRES. Aggressive postoperative management of blood pressure and the institution of anticonvulsant therapy were undertaken. The patient made a good recovery; however, he required a temporary tracheostomy and tube feedings for prolonged lower cranial nerve dysfunction. Posterior reversible encephalopathy syndrome can occur as a result of severe hypertension during surgery, even among young children. With prompt treatment, the patient in the featured case experienced significant clinical and radiographic recovery.

Isolated brainstem involvement in a patient with hypertensive encephalopathy.

Hypertensive encephalopathy (HE) is one of the acknowledged hypertensive emergencies. Isolated hypertensive brainstem encephalopathy (HBE) without concomitant typical parietooccipital lesion is unusual. Patients with HBE may or may not present with symptoms attributable to brainstem and the diagnosis is challenging in an emergency setting. The most important differential diagnosis in HBE is brainstem infarction, because the goals of blood pressure treatment are different. Evidence of vasogenic edema on magnetic resonance image, i.e. absence of high signal lesions on diffusion weighted images and increased value of apparent diffusion coefficient are diagnostic indicators of HBE, but not brainstem infarction. Prompt recognition of HBE and adequately lowering blood pressure offer the best outcomes.

Protease-activated receptor 2 and bradykinin-mediated vasodilation in the cerebral arteries of stroke-prone rats.

Protease-activated receptor 2 (PAR(2)) expression is up-regulated during vascular injury associated with edema. PAR(2) and bradykinin subtype 2 receptor (B(2)) expression and function were assessed in relation to hypertensive encephalopathy (HE) and cerebral hemorrhage (CH) in middle cerebral arteries (MCA) of Kyoto Wistar stroke-prone spontaneously hypertensive rats (SHRsp). Before stroke, bradykinin and PAR(2) activation by 2-furoyl-leucine-isoleucine-glycine-arginine-leucine-ornithine-amide (2Fly) produced endothelium-dependent vasodilation that was inhibited by K(+) depolarization, carbenoxolone, and the blockade of intermediate (IK(Ca)) plus small (SK(Ca)) and (in the case of bradykinin) smooth muscle (SM) large conductance (BK(Ca)) calcium-activated K(+) channels. Responses were not altered by N omega-nitro-L-arginine methyl ester, indomethacin, 17-octadecynoic acid or Ba(2+)+ouabain. We concluded that vasodilation to 2Fly or bradykinin was not mediated by NO, cyclooxygenases, arachidonic acid-metabolizing cytochrome P450s or SM K(ir) channels+Na(+)/K(+) ATPase activation. Vasodilation likely involved the spread of endothelial hyperpolarization (generated by IK(Ca)+SK(Ca)) through myoendothelial junctions and in some cases SM BK(Ca) activation. SHRsp with HE or CH had MCA that could not constrict to pressure and did not vasodilate to bradykinin. Their responses to 2Fly remained unaltered. The patterns and densities of PAR(2) and B(2) immunoreactivity in frozen MCA sections were not altered with stroke. MCA function remained normal in SHRsp subjected to dietary manipulations that prevented stroke without altering hypertension. Despite the presence of vascular injury, edema, inflammation and the loss of endothelium-dependent bradykinin vasodilation we found no evidence that PAR(2) expression or vascular function was altered in MCA after stroke.