Migraine and hypertension.

Association between mild to moderate hypertension and headache is probably coincidental. Severe sustained hypertension, malignant hypertension and paroxysmal hypertension (sudden rise) are associated with severe headache. Transient hypertension can occur during an attack of migraine or cluster headache. Hypertension may increase the frequency and severity of migraine in migraineurs and may transform an episodic migraine into chronic daily headache. Concomitant treatment of hypertension is important in these patients.

Coexistence of migraine and idiopathic intracranial hypertension without papilledema.

Eighty-five patients with refractory transformed migraine type of chronic daily headache (CDH) had spinal tap as a part of diagnostic work-up. Twelve had increased intracranial pressure without papilledema, transient visual obscurations, or visual field defects. The headache profile of these 12 patients was not different from that of transformed migraine type of CDH. Acute headache exacerbations responded to specific antimigraine agents such as ergotamine, dihydroergotamine (DHE), and sumatriptan, whereas prophylactic antimigraine medications were only partially helpful. Addition of agents such as acetazolamide and furosemide, after the diagnosis of increased intracranial pressure, resulted in better control of symptoms. These observations suggest a link between migraine and idiopathic intracranial hypertension that needs further research. In refractory CDH with migrainous features, a spinal tap to exclude coexistent idiopathic intracranial hypertension without papilledema may be indicated.

Severe diffuse intracranial vasospasm as a cause of extensive migrainous cerebral infarction.

We report on a 47-year-old white female with a long history of recurrent episodes of migraine with aura, who progressed to develop a continuous intractable headache during the course of which cortical blindness and quadriparesis occurred due to extensive and bilateral hemispheric cerebral infarction. Severe diffuse intracranial major arterial vasospasm was demonstrated by arteriogram. All studies were negative for CNS vasculitis, including cerebral biopsy. The arterial spasm reversed itself, but the patient did not improve. Smoking was the only additional risk factor. Vasospasm is an important cause to be considered in migrainous infarctions. The use of vasoconstrictor agents such as DHE in patients with migraine with prolonged aura has to be carefully re-evaluated.

Drug-induced headache.

Headache induced by medications used for nonheadache conditions, and more importantly, headache perpetuated by symptomatic medications used for primary headache disorders are discussed in detail in this article. The clinical features and mechanisms of drug-induced headaches are reviewed. Ergotamine and analgesic rebound phenomena are described. Management strategies for drug-induced headaches are outlined.

Hyperlipidemic neuropathy and dementia.

Mixed types of sensory and motor peripheral neuropathy and dementia occurred as neurological complications in patients with established type IV and type V hyperlipoproteinemia. These complications were remedial by control of the hyperlipoproteinemia with diet and/or clofibrate resulting in symptomatic improvement as well as restitution of nerve conduction velocities toward normal. Diabetes mellitus as well as systemic metabolic and toxic disorders which commonly produce neurological complications were excluded. Segmental demyelination with disorganization of myelin lamellae were striking morphological features found on sural nerve biopsy. Fluctuations in memory performance correlated inversely with plasma lipid levels and appear to be a characteristic feature of hyperlipidemic dementia. Hyperlipidemic neuropathy and dementia, although rare, are remediable neurological disorders which should be considered in patients with neuropathy and/or dementia of unknown origin.

Increased cerebral blood volume in benign intracranial hypertension.

In two patients with benign intracranial hypertension, the regional cerebral blood volume was markedly elevated (mean of 85 percent) while regional cerebral blood flow was slightly reduced (mean of 10 percent). Reduction of cerebrospinal fluid pressure by removal of cerebrospinal fluid reduced the mean values of regional cerebral blood volume by 13 percent without significant change in regional cerebral blood flow. The abnormal regional volume and regional flow returned to normal concurrent with the clinical improvement. Vinous engorgement and increased intracranial blood volume appear to play an important part in the pathophysiology of increased intracranial pressure in benign intracranial hypertension. A unified concept of the pathogenesis of benign intracranial hypertension is proposed.

PIP: 2 women complaining of headaches were found to have benign intracranial hypertension with increased rCBV (regional cerebral blood volume) of 85% and reduced rCBF (regional cerebral blood flow) of 10%. A lumbar puncture was done showing a small rCBV reduction of 13% but no significant change in rCBF. The patients were also administered 1.5 gm/kilogram body weight of glycerol 3 times a day. After 18 weeks of glycerol treatment, headaches and papilledema disappeared, rCBV and rCBF returned to normal levels, and cerebrospinal fluid pressure was reduced. It is believed that all 3 intracranial compartments may be involved in producing intracranial pressure in benign intracranial hypertension patients although it is difficult to determine the varying degrees to which each factor may be involved. The intracranial pressure may be increased due to venous engorgement and increased CBV. Because of undesirable side effects after long term use of deramethasone and diuretics like furosemide, oral glycerol therapy is used for prolonged therapy without adverse reactions.

Late complications of hemispherectomy: report of a case relieved by surgery.

A case of Sturge-Weber disease treated with left hemispherectomy presented, 11 years later, with complications related to delayed intracranial haemorrhage. A loculation syndrome of the right lateral ventricle was detected and it was corrected by a ventriculoatrial shunt operation. The side of the hemispherectomy was evacuated of all the chronic products of haemorrhage, including the subdural membrane. The patient was relieved of her symptoms. It is considered that complications related to delayed haemorrhage after hemispherectomy are remediable.