Alessandro S. Zagami

Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis.

To describe a distinctive seizure semiology that closely associates with voltage‐gated potassium channel (VGKC)‐complex/Lgi1 antibodies and commonly precedes the onset of limbic encephalitis (LE).

The neuropsychological profile of vascular cognitive impairment in stroke and TIA patients.

Objective: To characterize the neuropsychological profile of vascular cognitive impairment (VCI) and vascular dementia (VaD). Methods: The authors examined 170 patients with stroke or TIA at 3 to 6 months after the vascular event, and 96 age-matched healthy controls, with detailed neuropsychological and medical-psychiatric assessments, with a majority (66.7%) undergoing MRI brain scans. The subjects were diagnosed as having VaD, VCI, or no cognitive impairment by consensus. The neuropsychological tests were classified into cognitive domains, and composite z-scores adjusted for age and education. Results: VaD subjects had disturbance in all cognitive domains, with verbal memory, especially retention, being less affected. VCI subjects had similar but less severe disturbance. The domains that best discriminated cognitively impaired from unimpaired patients were abstraction, mental flexibility, information processing speed, and working memory. Cognitive impairment had a significant correlation with deep white matter hyperintensities, but not with volume and number of infarctions, even though the VaD subjects had larger infarct volumes than VCI subjects. The MRI variables did not provide additional discrimination between subgroups. Conclusions: The cognitive deficits in VaD and VCI are characterized by disturbance of frontal functions, with less verbal memory impairment. VaD and VCI differ in severity but not pattern of disturbance. The brain lesions that best account for these deficits are noninfarct subcortical white matter and gray matter changes due to ischemia. The picture of VaD/VCI presented shows subcortical deficits embellished by cognitive deficits from cortical infarctions.

Stimulation of the superior sagittal sinus in the cat causes release of vasoactive peptides

External jugular vein blood was sampled in the anesthetized cat during electrical stimulation of the superior sagittal sinus (SSS), and the levels of calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), substance P (SP) and neuropeptide Y (NPY) were measured with sensitive radioimmunoassays. CGRP levels rose by 85% and VIP levels by 300% while there was no change in SP or NPY levels in the same samples. These data provide the first evidence that activation of the trigeminovascular system, by selective stimulation of nociceptive craniovascular afferents, causes releases of vasodilator peptides and further implicates this system in the pathophysiology of migraine.

Neural Processing of Craniovascular Pain: A Synthesis of the Central Structures Involved in Migraine

SYNOPSIS

STIMULATION OF THE MIDDLE MENINGEAL ARTERY LEADS TO FOS EXPRESSION IN THE TRIGEMINOCERVICAL NUCLEUS : A COMPARATIVE STUDY OF MONKEY AND CAT

The pain of a migraine attack is often described as unilateral, with a throbbing or pulsating quality. The middle meningeal artery (MMA) is the largest artery supplying the dura mater, is paired, and pain‐producing in humans. This artery, or its branches, and other large intracranial extracerebral vessels have been implicated in the pathophysiology of migraine by theories suggesting neurogenic inflammation or cranial vasodilatation, or both, as explanations for the pain of migraine. Having previously studied in detail the distribution of the second order neurons that are involved in the transmission of nociceptive signals from intracranial venous sinuses, we sought to compare the distribution of second order neurons from a pain‐producing intracranial artery in both monkey and cat. By electrically stimulating the middle meningeal artery in these species and using immunohistochemical detection of the proto‐oncogene Fos as a marker of neuronal activation, we have mapped the sites of the central trigeminal neurons which may be involved in transmission of nociception from intracranial extracerebral arteries. Ten cats and 3 monkeys were anaesthetised with α‐chloralose and the middle meningeal artery was isolated following a temporal craniotomy. The animals were maintained under stable anaesthesia for 24 h to allow Fos expression due to the initial surgery to dissipate. Following the rest period, the vessel was carefully lifted onto hook electrodes, and then left alone in control animals (cat n = 3), or stimulated (cat n = 6, monkey n = 3). Stimulation of the left middle meningeal artery evoked Fos expression in the trigeminocervical nucleus, consisting of the dorsal horn of the caudal medulla and upper 2 divisions of the cervical spinal cord, on both the ipsilateral and contralateral sides. Cats had larger amounts of Fos expressed on the ipsilateral than on the contralateral side. Fos expression in the caudal nucleus tractus solitarius and its caudal extension in lamina X of the spinal cord was seen bilaterally in response to middle meningeal artery stimulation. This study demonstrates a comparable anatomical distribution of Fos activation between cat and monkey and, when compared with previous studies, between this arterial structure and the superior sagittal sinus. These data add to the overall picture of the trigeminovascular innervation of the intracranial pain‐producing vessels showing marked anatomical overlap which is consistent with the often poorly localised pain of migraine.

Clinical Determinants of Dementia and Mild Cognitive Impairment following Ischaemic Stroke: The Sydney Stroke Study

Background: Dementia following stroke is common but its determinants are still incompletely understood. Methods: In the Sydney Stroke Study, we performed detailed neuropsychological and medical-psychiatric assessments on 169 patients aged 50–85 years, 3–6 months after a stroke, and 103 controls with a majority of both groups undergoing MRI brain scans. Stroke subjects were diagnosed as having vascular mild cognitive impairment (VaMCI) or vascular dementia (VaD) or no cognitive impairment by consensus. Demographic, functional, cerebrovascular risk factors and neuroimaging parameters were examined as determinants of dementia using planned logistic regression. Results: 21.3% of subjects were diagnosed with VaD, with one case in those aged 50–59 years, 24% in those aged 60–69 years and 23% in those 70–79 years. There was no difference by sex. The prevalence of VaMCI was 36.7%. VaD subjects had lower premorbid intellectual functioning and had 0.9 years less education than controls. The VaD and VaMCI groups did not differ from the no cognitive impairment group on any specific cerebrovascular risk factor, however overall those with impairment had a greater number of risk factors. They did not differ consistently on depression severity, homocysteine levels and neuroimaging parameters (atrophy, infarct volume and number of infarcts) except for an excess of white matter lesions on MRI and greater number of infarcts in the VaD and VaMCI groups. On a series of logistic regression analyses, stroke volume and premorbid function were significant determinants of cognitive impairment in stroke patients. Conclusion: Post-stroke dementia and MCI are common, especially in older individuals. Cerebrovascular risk factors are not independent risk factors for VaD, but stroke volume is a significant determinant of dementia. Premorbid functioning is a determinant of post- stroke impairment.

Oral sumatriptan in acute migraine

The efficacy in acute migraine of oral sumatriptan was assessed in a double-blind, randomised, placebo-controlled, crossover study of 61 patients (mean age 39 [SD 10] years). 41 completed treatment of four attacks, two with sumatriptan 100 mg and two with placebo. The response rate (reduction in headache from moderate or severe to mild or absent at 2 h) was 51% (45/89) with sumatriptan and 10% (9/93) with placebo (p less than 0.01); rescue medication was needed at 2 h in 41% and 88%, respectively. Of 28 patients headache-free at 24 h, 11 (39%) had recurrent headache within 24 h. There were no substantial side-effects. Thus, sumatriptan is an effective well-tolerated treatment for acute migraine attacks.

The Mode of Action of Migraine Triggers: A Hypothesis

Objectives.— To review conjectured modes of action of migraine triggers and to present a new hypothesis about them.

Ophthalmoplegic migraine: a recurrent demyelinating neuropathy?

The demonstration by magnetic resonance imaging (MRI) scanning of thickening and enhancement of the cisternal part of the oculomotor nerve in patients diagnosed as ‘ophthalmoplegic migraine’ prompts reconsideration of this uncommon disorder. The case histories of five patients, three male and two female, varying in age from 6 to 30 years, are presented here. Recurrent painful ophthalmoplegia started in infancy in two cases, childhood in two instances and adult life in one. One child had his first attacks at 3, 5 and 12 months of age, on each occasion 10 days after an injection of triple vaccine. The possibility of this condition being a recurrent demyelinating neuropathy is considered and its possible relationship to migraine explored.

Stimulation of cranial vessels excites nociceptive neurones in several thalamic nuclei of the cat

SummaryExtracellular recordings were made in the thalamus of cats anaesthetized with chloralose and urethane following electrical, mechanical and chemical stimulation of the superior sagittal sinus or middle meningeal artery. Facial receptive fields were looked for using electrical and mechanical stimuli. The locations of fifty-six cells were verified histologically. Twenty six cells were located in the ventroposteromedial nucleus (VPM) and six in its ventral periphery (VPMvp). All units in VPM had facial receptive fields, usually involving the first trigeminal division. Cells with nociceptive receptive fields or responding to the craniovascular application of bradykinin were often found in the periphery or “shell” region of VPM. Other craniovascular nociceptive cells were found in VPMvp, in the posterior group and in the intralaminar complex. This study shows that craniovascular afferents in the cat project to several thalamic nuclei and implicate VPM especially in craniovascular nociception.