OCR Text |
Show 124 1. M. WILLIAMS tion revealed lymphocytosis, and symptomatic intracranial hypertension was suggested by CSF manometry,' mild optic disc swelling, and headache promptly relieved by lumbar puncture. Although vision remained poor, headache was controlled by corticosteroid medication. The authors stated th~t this condition has been reported in association with CSF pleocytosis and cerebral vasculitis, but not previously documented in association with intracranial hypertension. t 5. Professor Michael Anthony, in his paper entitled The Roll' o{ the Occipital Nape ill Headache, stated that disturbances in the upper cervical spine have been known to cause pain in both the occipital and frontotemporal areas of the head. The mechanism suggested was irritation of nerves in that area, and 111 particular of the greater occipital. To test this hypothesis, methyl-prednisolone acetate (Depo-Medrol) was injected into the region of the greater occipital nerve ipSilateral to the headache to patients suffering from (a) a bout of cluster headaches, (b) frequent unilateral migraine attacks, and (c) pain of occipital neuralgia. Relief was said to be expenenced by (a) 18 of the 20 patients with cluster headache for 5-73 days, (b) 18 of the 20 patients with migraine for 13-66 days, and (c) 19 of the 20 patients with occipital neuralgia for 28-140 days. According to Professor Anthony, it is generally accepted that the central connections between the trigeminal nerve and the upper three cervical roots (the components of the greater occipital nerve) form the pain center for the head. If attacks of headache such as those described are due to paroxysmal activity of this center as a result of impulses received from its many connections, it appears that impulses arriving along the greater occipital nerve are the most significant, and therefore their interruption leads to pain relief more regularly than interruption of other neural pathways employed so far. t 6. Drs. K. J. Abbott, P. F. Weston, and J. I. Manson, in their paper Predicting Optic Nape Damage from Raised Intracranial Pressure Using the Pattem VisualEvoked Response, maintained that clinical testing may fail to identify those patients with papilledema at serious risk of visual deterioration. They found subclinical optic nerve dysfunction, detected by the pattern visual-evoked response, had seldom been reported in this context. In their study, 30 children (age range 2.7-15.5 years) presenting with papilledema from raised intracranial pressure had monocular pattern visual evoked response studies at diagnosis, most having follow-up tests. None had lesions causing infiltration or tumour compression of visual pathways. Initial studies were normal in 25 (83%), all of whom maintained their normal pretreatment vision; one child with pattern visual-evoked response latencies at the , .. '", ," ·...·...nl'hllra!.lIol. Vol. 6. No.2, 1986 t 7. * 8. upper limit of normal ha~ subcli.nical optic neuropathy on later testing. Five patle~ts (ages 7-13.5 years) had abnormal pattern Visual evoked responses, without visual loss, in one or both. eyes. Optic nerve function recovere~ after corre.chon of increased intracranial pressure 111 three of five, one case having transient monocular visual deterioration (initial PI latency 121 ms, N < 116 ms). Two patients with significant pattern visual-evoked response latency delays at pres.entation ~evelop.ed secondary optic atrophy despite correction of 111tracranial pressure. Papilledema due to raised intrac.ranial pressure alone seldom affects the pattern Visual-evoked response. Significant pattern visual-evoked respon~e latency delay implies a high risk of secondary optic neuropathy despite normal clinical vision. Patte~ visual-evoked response testing may be useful 111 certain preoperative cases with raised intracranial pressure and in patients with pseudotumour cerebri. Drs. E. Byrne, I. Trounce, and X. Dennett presented a paper on Partial Cytochrome Oxidase Deficimclj in Chronic Extemal Ophthalmoplegia describing biochemical and histochemical studies which were carried out in hvo patients with chronic progressive external ophthalmoplegia. Both patients had associated proximal myopathy and one patient had a pigmentary retinopathy. Histological findings were similar in both cases with prominent ragged red fibers (Gomori Trichrome stain) and partial deficiency of cvtochrome oxidase staining with a negative r~acti~n in many ragged red and occasional morphologically normal fibers. Cytochrome oxidase levels were greatly depressed in muscle homogenate in both cases. A cytochrome oxidation/reduction spectrum was recorded in one case and revealed a severe deficiency of cytochrome a/aa,. Polarographic studies with isolated skeletal muscle mitochrondia revealed depressed state 3 respiration rates with flavoprotein and nicotinamide adenine dinucleotide-linked substrates. Histochemical data and biochemical investigation using three different approaches therefore confirm a partial cytochrome oxidase deficiency in some patients with partial cytochrome oxidase deficiency in chronic external ophthalmoplegia. It is not established whether cytochrome oxidase deficiency is central to disease pathogenesis or is an epiphenomenon in mitochondrial degeneration of another cause. Drs. B. Fenelon, K. Grant, A. Delahunty, R. Neill, D. Dunlop, P. Dunlop, B. Frost, and A. Quayle, in their paper Global Stereopsis in Stroke Patients, stated that contradictory evidence has appeared in the literature on the possible existence of a right hemisphere mechanism subserving global stereopsis. Their study was aimed at clarifying the issue by |