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Biomedical subjects

G J Hankey

Publications and source records attributed to G J Hankey.

At least 109 records · Page 6Linked to original sources

Cervical myelopathy due to calcification of the ligamentum flavum.

An elderly Caucasian woman presented with a cervical myelopathy due to cervical spinal cord compression posteriorly by calcified ligamentum flavum and anteriorly by cervical osteophytic bars. Although recognized in the Japanese population, calcification of the ligamentum flavum as a cause of cervical myelopathy is very rare in Caucasians, with only one case previously reported.

Aged↗

Median nerve compression in the palm of the hand by an anomalously enlarged ulnar artery.

Median nerve compression in the carpal tunnel by a thrombosed persistent median artery and a large aberrant artery substituting for the radial artery has been described but there have been no reports of median nerve compression in the palm of the hand by an anomalously enlarged ulnar artery. A 46 year old man is described who presented with clinical and electrophysiological features consistent with a median neuropathy at the wrist but surgical exploration revealed median nerve compression in the palm of the hand by an anomalously enlarged palmar branch of the ulnar artery. This case highlights another treatable cause of median nerve compression and illustrates that symptoms suggestive of carpal tunnel syndrome may be produced by median nerve compression in the palm of the hand.

Arteries↗

Amnesia following thalamic hemorrhage. Another stroke syndrome.

The clinical manifestations of thalamic hemorrhage frequently comprise hemiparesis, hemianesthesia, and oculomotor abnormalities. Since the advent of computed tomography, an amnestic syndrome following thalamic hemorrhage has been recognized, but the thalamic structures involved and the mechanism of amnesia have remained uncertain. We report a patient with sudden memory dysfunction following hemorrhage into the anterior nucleus of the left thalamus that was shown neuropathologically to disrupt the mamillothalamic fasciculus, one of the principal components of the limbic system. It is considered that the amnestic syndrome following thalamic (anterior nucleus) hemorrhage is due to interruption of the mamillothalamic fasciculus.

Amnesia↗

Five cases of sudden hearing loss of presumed vascular origin.

Sudden hearing loss is an important symptom which demands immediate evaluation. Although it may be attributed to a number of disorders, relatively few clinicopathological correlations have been described. The role of vascular disease in the aetiology of sudden hearing loss has been acknowledged in several case reports, but remains unclear and perhaps underemphasized, given the prevalence of vascular disease in other organ systems in Western communities. Five cases of sudden hearing loss due to presumed vascular disease are reported. It is postulated that vascular disease is an important factor in the pathogenesis, and one which may be overlooked in the management of sudden hearing loss.

Adult↗

Focal cerebral ischaemia and infarction due to antihypertensive therapy.

Eight cases of postural focal cerebral ischaemia due to antihypertensive medications presented to one neurologist over an eight-month period. Most patients were elderly and suffered from chronic hypertension; their symptoms resolved after the reduction or cessation of these medications. These findings re-emphasize that considerable caution is required when antihypertensive medications are used in elderly persons and in patients with chronic hypertension whose cerebral blood-flow autoregulatory curves are shifted to the right. We also draw attention to the fact that drug-induced hypotension may induce focal cerebral ischaemia rather than generalized cerebral ischaemia more frequently than is generally appreciated.

Adult↗

Guillain-Barré syndrome in Western Australia, 1980-1985.

A clinicoepidemiological study of 109 patients with Guillain-Barré syndrome who were admitted to the four major teaching hospitals in Perth between January 1, 1980 and December 31, 1985 was conducted through the Hospital Morbidity Data System. The annual incidence rate of Guillain-Barré syndrome was 1.35 cases per 100,000 population. The age-adjusted incidence rates were 1.49 cases per 100,000 men and 1.20 cases per 100,000 women. A minor peak in the sex-adjusted incidence rate was present in young adult life with a larger peak in later life. Twenty-two (20%) patients presented in the five-month period from July 1984 to November 1984 (P less than 0.05) but a common infectious agent or geographical area of residence was not discovered during this period. Immune function had been affected potentially before the onset of Guillain-Barré syndrome in 12 (11%) patients, which raises further speculation as to the role of immunological mechanisms in the pathogenesis of Guillain-Barré syndrome. In order to enhance our understanding of this disorder, it is recommended that an assessment of immune function be considered in cases of Guillain-Barré syndrome and also chronic inflammatory demyelinating polyneuropathy.

Adult↗

Peliosis hepatis in a renal transplant recipient and in a haemodialysis patient.

Peliosis hepatis is described in a renal transplant recipient and in a patient who was receiving long-term haemodialysis. This uncommon liver lesion has been reported in a number of patients, including 18 renal transplant recipients and two patients with chronic renal failure. However, its cause, clinical features, natural history and clinical significance remain to be determined. We emphasize that, although it is rare, peliosis hepatis should be considered in long-term haemodialysis and renal transplant patients who exhibit hepatomegaly and/or splenomegaly and/or disordered liver function (in particular, elevation of hepatic alkaline phosphatase levels).

Adult↗

Asymptomatic cerebellar venous angioma.

In contrast to the scarcity of recorded cases of radiologically studied venous angiomas, venous angiomas are the most common of the four basic types of congenital intracranial vascular malformations encountered incidentally at autopsy. Their clinical significance remains unclear. When symptomatic, they are associated mainly with hemorrhage or mechanical pressure on cranial nerves by anomalously enlarged veins, however, it is, as yet, impossible to predict what course an asymptomatic cerebellar venous angioma will take. The risks of surgery appear to exceed those of the natural history of the disorder. The following two cases of asymptomatic cerebellar venous angioma are recorded because of the rarity of the condition's diagnosis and the possibility of controversy in its conservative management.

Adult↗

Chiasmal apoplexy due to intrachiasmatic vascular malformation rupture.

Hemorrhage from an intrinsic vascular malformation of the optic chiasm (chiasmal apoplexy) is an uncommon cause of sudden visual loss with chiasmal visual field defects. This paper describes one case of sudden visual loss with an anterior chiasmal visual field defect due to rupture of an intrachiasmatic venous angioma and contrasts it with the clinical presentation of a case of hemorrhage from an intrachiasmatic arteriovenous malformation causing severe headache and a less apoplectic onset of visual symptoms. The variable clinical presentation and the accuracy of high resolution post-contrast cranial CT scan in the diagnosis of intrachiasmal hemorrhage is highlighted.

Adult↗

Localising value of primary position upbeating nystagmus.

Primary position upbeating nystagmus has been associated clinically with intra-axial brainstem and cerebellar lesions but evidence for more precise localisation to the ponto-mesencephalic and ponto-medullary junctions is accumulating. We report the occurrence of primary position upbeating nystagmus in three patients who had clinical signs of pontine lesions at the ponto-mesencephalic and ponto-medullary junctions. Radiological confirmation was possible in two cases.

Adult↗

Orbital myositis: a study of six cases.

Orbital myositis implies orbital inflammation confined to one or more of the extraocular muscles. Orbital computerised tomography (CT) demonstrates irregular extraocular muscle enlargement which extends anteriorly to involve the tendon (muscle insertion). Six cases of presumed orbital myositis are reported, in each of whom the diagnosis was suspected clinically and confirmed by the orbital CT scan appearances. The mean age of the patients was 33 years (range 8-45 years). All presented with painful ophthalmoplegia and the majority manifested proptosis (five cases), conjunctival congestion (five cases) and periorbital and eyelid edema (two cases). Systemic corticosteroid therapy was used in two patients initially and also in another patient who relapsed, with rapid and dramatic responses. Extraocular muscle biopsy was performed in one case, disclosing features of non-specific muscle inflammation and no evidence of vasculitis. It is considered that orbital myositis is a discrete, identifiable subgroup within the spectrum of the nonspecific idiopathic orbital inflammatory syndromes; termed previously orbital 'pseudotumours'. Although the clinical features are frequently suggestive, they are nonspecific, and non-invasive investigations such as orbital ultra-sonography and CT scanning are required for precise anatomical tissue localisation and diagnosis. The role of ocular muscle biopsy is probably limited to atypical cases, or those unresponsive to steroid therapy, particularly to exclude neoplasia. Orbital myositis may be acute, subacute or recurrent. The acute form responds well to high doses of oral corticosteroids tapered gradually, but it may recur or become chronic. The subacute form of the disease responds less well.

Adult↗