[Anatomical and neurochemical bases accounting for the frequent association between headaches and sleep: the hypnic headache paradigm]. / Bases anatomicas y neuroquimicas que explican la frecuente asociacion de las cefaleas con el sueno: el paradigma de la cefalea hipnica.

INTRODUCTION: The relationship between headache and sleep is complex and runs in two directions. Headache may be the consequence of a (primary or secondary) sleep disorder or its cause (in chronic tension-type headache and/or chronic migraine with or without painkiller abuse). It can also be related to sleep in an intrinsic way, as in the case of hypnic headache (which only appears during sleep) or other primary headaches, such as migraine and certain trigeminal-autonomic cephalgias (which can appear during the waking state or during sleep); this type of headache occurs mostly during REM sleep. DEVELOPMENT: The neural pathways that control sleep and pain are anatomically, physiologically and neurochemically cross-linked. These neural systems are located in the brain stem, the hypothalamus and the basal brain. Such cross-links are produced on two different levels. On the one hand, they occur in the serotoninergic nuclei of the brain stem, whose activity in physiologically diminished during REM sleep and which are involved in antinociceptive control. On the other hand, they are also to be found in the hypothalamus, where serotoninergic terminals have been detected in the suprachiasmatic nucleus (SCN). As cells in the SCN are lost with age, their circadian and homeostatic functioning fails, the activity of the hypothalamus-pineal axis is reduced and the endogenous melatonin rhythm is altered. This results in a disorder affecting the control of the sleep-waking cycle and antinociceptive control. CONCLUSIONS: Dysfunctions in these neuronal networks in the brain stem (especially in the serotoninergic nuclei) or the hypothalamus (SCN) can account for headaches that begin in the REM phase of sleep and affect biologically predisposed subjects.

[Wallenberg syndrome as a sign of rhombencephalitis-meningitis due to Listeria monocytogenes]. / Síndrome de Wallenberg como manifestación de meningorrombencefalitis por Listeria monocytogenes.

We report a case of rhombencephalitis with meningitis in a 36-years-old previously healthy man; neurological signs and symptoms were initially consistent with a diagnosis of Wallenberg syndrome. Analysis of cerebrospinal fluid showed predominantly lymphocytic pleocytosis and elevated protein levels. A CT brain scan was normal. MRI of the brain showed a hypertensive type lesion in T2, in the right pontomedullary region that suggested inflammation. A blood culture grew Listeria monocytogenes. The patient improved and fully recovered with appropriate antibiotic treatment. Listeria monocytogenes is a recognized cause of acute brainstem meningoencephalitis. Differential diagnoses that must be considered are other forms of purulent meningitis, viral meningoencephalitis, granulomatosis infections of the central nervous system and, occasionally, stroke.

Small arterial granular degeneration in familial Binswanger's syndrome.

A 55-year-old mildly hypertensive woman died after having developed a subcortical dementia during the past 9 years, with focal neurological signs. She presented at the age of 46 years with short episodes of dizziness and diplopia, suggesting that transient ischemic attacks involved the posterior fossa structures. Over the next 8 years, she developed difficulty in walking, urinary incontinence and seizures. On examination in 1989, she was severely demented. There was tetraparesis, bilateral arm and leg spasticity with hyperreflexia and bilateral Babinski signs. She showed epilepsia partialis continua involving the eyes, left hemiface and limbs. CT showed hypodensity of the white matter and lacunes in the basal ganglia and centrum semiovale, moderate hydrocephalus with cerebellar and cortical atrophy. Clinical and radiological features were similar to those of Binswanger's disease. Similar cases had occurred in the family affecting the patient's grandfather, father and two brothers, suggesting an autosomal dominant hereditary disease. Postmortem examination disclosed a Binswanger type of leukoencephalopathy caused by a peculiar microangiopathy characterized by a slightly basophilic small arterial granular degeneration of the medial sheath associated with the presence of ballooned smooth muscle cells with clear cytoplasm. Electron microscopic study revealed degenerative changes in the parietal vessels with notable increase of basal-membrane-type material and electron-dense granular deposits. These lesions could correspond to a specific familial pathology of the small arteries of the brain. They are identical to those reported in some patients with autosomal dominant inheritance. For other patients with similar clinical features and the same familial pattern, reported as "hereditary multi-infarct dementia'' and "chronic familial vascular encephalopathy'', there are no sufficient objective pathological facts to consider that they have the same disease.(ABSTRACT TRUNCATED AT 250 WORDS)