Sir Winston Churchill: treatment for pneumonia in 1943 and 1944.

This paper reviews Churchill's illnesses in February 1943 and August/September 1944 when he developed pneumonia; on the first occasion this followed a cold and sore throat. Churchill was managed at home by Sir Charles Wilson (later Lord Moran) with the assistance of two nurses and the expert advice of Dr Geoffrey Marshall, Brigadier Lionel Whitby and Colonel Robert Drew. A sulphonamide (sulphathiazole on the first occasion) was prescribed for both illnesses. Churchill recovered, and despite his illnesses continued to direct the affairs of State from his bed. On the second occasion, Churchill's illness was not made public.

In Carthage ruins: the illness of Sir Winston Churchill at Carthage, December 1943.

This paper reviews Churchill's illness in Carthage in December 1943. It was characterised by fever that lasted 6 days, left lower lobe pneumonia and two episodes of atrial fibrillation. He was managed in a private villa by Lord Moran, his personal physician, with the assistance of two nurses and the expert advice of colleagues. Sulphadiazine and digitalis leaf were prescribed and Churchill recovered. It is remarkable that, despite the severity of his illness, he continued to direct the affairs of State from his bed.

Central nervous system sarcoidosis--diagnosis and management.

A series of 68 patients with neurosarcoidosis is reported, with particular emphasis on clinical aspects, diagnosis and treatment. A classification system based on clinical diagnostic probability is proposed, consisting of probable and definite disease, the latter being dependent on finding sarcoid granulomas on nervous system histology, which was obtained in 12 patients (18%). The role of investigations, including magnetic resonance imaging (MRI), chest radiography, Kveim skin test, Gallium 67 isotope scanning and cerebrospinal fluid (CSF) studies, is considered. Sixty-two percent of patients presented with nervous system disease, most commonly affecting the optic nerve and chiasm. Other common presentations included cranial nerve palsies, spinal cord and brainstem manifestations. Investigations yielding most diagnostic information included the Kveim test (41/48, 85% positive), raised CSF protein and/or cells (50/62, 81%) and gallium 67 scan (14/31, 45%). Eleven out of 29 patients (38%) patients showed meningeal enhancement on MRI scanning and 43% of scans demonstrated multiple white-matter lesions. Mean follow-up for the group was 4.6 years. Forty-seven patients were seen for > 18 months, and over half of these patients progressed despite corticosteroid and other immunosuppressive therapies. The benefit of a large patient database prospectively studied, with extended follow-up is discussed in order to learn more about prognosis and advance therapy in neurosarcoidosis.

Idiopathic spontaneous subdural hemorrhage.

We describe three middle-aged and previously healthy patients in whom idiopathic spontaneous subdural hemorrhage occurred, giving rise to headache with minimal or no neurological signs and resolving with conservative management. Previous reports of this condition describe an associated severe neurological impairment, a poor prognosis, and a necessity for surgical evacuation. Our cases indicate that mild and self-limiting spontaneous subdural hemorrhage may occur and is perhaps underdiagnosed in our patients' age group because it presents non-specifically with headache.

Posterior communicating artery aneurysm presenting with haemorrhage into an arachnoid cyst.

A patient is reported on with a subarachnoid haemorrhage (SAH) from an aneurysm of the posterior communicating artery, who initially presented with a sentinel bleed into an arachnoid cyst and normal magnetic resonance angiography (MRA) of the intracranial vasculature which led to a delay in diagnosis. Although this is a very rare presentation of a relatively common condition, it is important to recognise the importance of intracystic haemorrhage in such circumstances as well as the limitations of MRA, as a delay in diagnosis may have serious clinical consequences.

Ultrastructural localization of sympathetic axons in experimental rat sciatic nerve neuromas.

The ultrastructural localization of sympathetic axons was investigated in normal rat sciatic nerves and experimental sciatic nerve neuromas. The best ultrastructural localization of noradrenaline in the dense-cored vesicles of sympathetic axons was accomplished following pretreatment of rats with nialamide and 5-hydroxy dopamine, followed by fixation according to the modified chromaffin technique of Tranzer and Richards (1976). After such preparation, sympathetic axons containing 5-hydroxy dopamine-labelled dense-cored vesicles could be identified in normal sciatic nerve. Large accumulations of labelled dense-cored vesicles were also found in acute neuromas, up to 1 week after nerve section. Much smaller numbers of dense-cored vesicles could be identified in chronic neuromas from 2 to 3 weeks following nerve section. Sympathetic axons could also be identified following electron probe X-ray microanalysis of the tissue sections, using chromium detection as the marker for the noradrenaline-containing dense-cored vesicles. Unusual configurations of Schwann cell subunits, which enclosed myelinated fibres and sympathetic axon sprouts within the same basal lamina, were identified in the acute neuromas, 3-7 days after nerve section. Such configurations may be of relevance to the pathophysiological interaction which develops between sympathetic efferent and sensory fibres in peripheral nerve neuromas.

Alien hand sign in association with Alzheimer's histopathology.

A 68 year old man is described with an alien left hand, cortical myoclonus, bilateral parietal lobe dysfunction and memory impairment but preserved language skills. The clinical diagnosis was of corticobasal degeneration but at necropsy, four years after the onset of symptoms, the pathology was of Alzheimer's disease together with some scattered chromatolytic pale neurons in the cerebral cortex. The alien hand sign has not previously been described in Alzheimer's dementia and is an illustration of the clinical heterogeneity that may occur in association with Alzheimer histopathology.

Successful treatment of childhood onset symptomatic dystonia with levodopa.

Three patients with childhood onset symptomatic dystonia responded to levodopa. None fulfilled criteria for a diagnosis of "dopa responsive dystonia" (Segawa's disease). One may have had athetoid cerebral palsy for almost 25 years. All obtained dramatic and sustained benefit from levodopa therapy. A therapeutic trial of levodopa is advised in all patients in whom dystonia has developed in childhood or early adult life, regardless of suspected aetiology or duration of symptoms.

A fluorescence study of changes in noradrenergic sympathetic fibres in experimental peripheral nerve neuromas.

Experimental neuromas were produced in rats by sciatic nerve section and avulsion of the distal stumps. At intervals varying from 3 days to 8 weeks after nerve section, the developing neuromas were resected and processed for noradrenaline (NA) fluorescence microscopy by the sucrose-phosphate-glyoxylic acid (SPG) method. From serial longitudinal sections through the neuromas and the nerve proximally, counts of noradrenergic sympathetic axons were made, together with qualitative observations of axon sprouting and NA content. By 3 days after nerve section there was a massive sprouting of sympathetic axons, with increased NA content, particularly towards the distal tip of the neuroma. Axon counts remained high 1 week following section then fell to below normal levels at 2 weeks, returning towards normal 8 weeks after nerve section. These results are discussed in relation to the known pathophysiological interaction between sympathetic efferent and sensory afferent fibres, which develops in neuromas following nerve section.

Morphological changes in IgM paraproteinaemic neuropathy.

Sural nerve biopsies were examined from two patients with neuropathy associated with IgM kappa [anti-myelin-associated glycoprotein (MAG)] paraproteinaemia. Both nerves had a moderate loss of myelinated fibres. The pathology in one was of a chronic primary demyelinating type, in the other it was associated with axonal atrophy. Widened myelin (WM) was seen in both nerves affecting over 80% and 50% of myelinated fibres, respectively. The WM was associated with deposition of material which sometimes appeared granular but could also display a highly organised pattern, an appearance not previously described in these neuropathies. Granular material was also identified at the external surface of the Schwann cells of myelinated, but not of unmyelinated, fibres. WM was seen not only at the outer lamellae (a commonly observed site) but also at terminal myelin loops at the paranode, at Schmidt Lanterman incisures and at the inner and outer mesaxon. Material was also seen on the inner (adaxonal) Schwann cell surface. These are all sites associated with the presence of MAG. Other pathological features are described, including evidence of impairment of remyelination, abnormal Schwann cell/axon specialisations and the presence of tomaculous bodies. The implications of these findings are discussed.

Persistent rheumatic chorea.

A 79-year-old woman had rheumatic chorea that persisted after age 5 years and increased in severity at age 73. The continued chorea and late decompensation could have been due to incomplete functional resolution in the basal ganglia and decreasing reserve of striatal neurons with age. Sydenham's chorea persisting into late life has not been reported previously.

Morton's metatarsalgia. Clinical, electrophysiological and histological observations.

In an attempt to improve the accuracy of diagnosis, 16 patients suffering from Morton's metatarsalgia were investigated clinically and electrophysiologically. The histological findings were related to these observations. The precise aetiology of Morton's metatarsalgia remains obscure, but the findings are compatible with an entrapment syndrome. Nerve conduction studies have a place in the investigation of patients with atypical presentation of pain in the foot. Further refinement of the electrophysiological technique should be possible.

Retrograde growth of myelinated fibres in experimental neuromas.

Retrograde growth of myelinated fibre sprouts following section of mouse sural nerves has been investigated. The results indicate that many sprouts grow relatively long distances proximally along the nerve trunk. The largest number of such sprouts was observed at 10 weeks after nerve section, with a decrease by 9 months. It has been shown that the retrogradely growing sprouts arise within the neuroma and not more proximally on the nerve.

Clinical trial of propranolol in post-traumatic neuralgia.

In view of several case reports of relief of various neuralgias by propranolo, a double-blind cross-over trial using this drug was conducted in 10 patients with severe persistent pain and paraesthesiae following upper limb peripheral nerve injuries. The patients received up to 240 mg of propranolol per day. Only one patient reported pain relief, but this patient withdrew from the trial. An open trial of propranolol was conducted in 6 other patients with a variety of peripheral nerve lesions. Of these, neuroma tenderness was transiently reduced in one patient and the hyperaesthesia of a painful scar was relieved in another. Routine use of propranolol in such patients cannot be recommended.

The permanent anatomical effects of neonatal capsaicin on somatosensory nerves.

The effects of neonatal capsaicin on the fibre populations of peripheral somatosensory nerves have been investigated in adult mouse sural nerve and rat saphenous nerve. One or two doses of capsaicin, 50 mg/kg, given in the first few days of life, caused a permanent 50% reduction in the number of unmyelinated axons in mouse sural nerve and a 64% reduction in rat saphenous nerve, compared with untreated controls. Schwann cell sub-units were also reduced in number, and on average contained fewer axons than controls. The number and size distribution of myelinated fibres were not affected by capsaicin. Active degeneration was seen in only a few unmyelinated axons, and a small number of denervated Schwann cell bands was present. There were no signs of unmyelinated fibre regeneration. It is concluded that neonatal capsaicin produces selective degeneration of unmyelinated axons in the neonatal period which has effectively reached its full extent by early adult life.