A survey of denture identification marking within the United Kingdom.

AIM: To assess the attitudes of healthcare workers within the UK towards identification marking of removable prostheses, and quantify the frequency with which this is currently undertaken. DESIGN: A postal questionnaire-based study. SETTING: The study was undertaken within the UK between 2002 and 2006 and surveyed prosthodontists working in a wide range of clinical settings. SUBJECTS AND METHODS: Questionnaires were sent to two sample groups: 1. Specialists in prosthodontics registered on the GDC specialist list; 2. Nursing staff in elderly care homes within the locality of Glasgow. RESULTS: Return rate of questionnaires from prosthodontic specialists was high, with 119 from 160 (74%) completed and returned. 54.9% of prosthodontic specialists carried out complete denture marking in their clinical practice and 40.9% undertook identification marking of partial removable prostheses. The vast majority (81.0%) of specialists indicated that denture identification marking was a worthwhile procedure. Furthermore, 68.9% thought the introduction of some form of guideline would be beneficial. Differences in the frequency of denture marking existed between varying clinical environments. Denture marking was not undertaken by healthcare workers within any of the surveyed care homes. CONCLUSION: The overwhelming opinion of prosthodontic specialists within the UK promotes the use of denture marking as a routine procedure.

Isolated horizontal supranuclear gaze palsy as a marker of severe systemic involvement in Gaucher's disease.

Type 3 neuronopathic Gaucher's disease (GD3) is phenotypically heterogeneous. In many GD3 patients, progressive myoclonus and dementia dominate the illness, with death secondary to progressive CNS disease. We have designated this group as GD3a. We studied 14 children with Gaucher's disease, isolated horizontal supranuclear gaze palsy, and aggressive systemic disease, and designated this group as GD3b. In comparison with 13 children with type 1 non-neuronopathic Gaucher's disease, the GD3b children presented earlier, and were shorter, underweight, and more prone to cardiopulmonary, hepatic, and skeletal complications. One-half of the children died in childhood or adolescence of systemic complications. Patients with at least one copy of the mutation that causes substitution of asparagine for serine at amino acid 370 of glucocerebrosidase did not develop neurologic signs. Patients homoallelic for the mutation causing substitution of leucine for proline at position 444 had severe systemic disease; neurologic signs were frequently, but not invariably, present. Early diagnosis and timely enzyme replacement therapy promise to improve the prognosis in GD3b.

HIV-related neurological disease.

Early neurological complications present an opportunity to make an early diagnosis of HIV infection. Patients may present with subtle symptoms and signs of neurological disease, but many HIV-related complications are readily treated if they are correctly diagnosed. As there are also neurological side effects of anti-HIV drugs, the management of patients with neurological complications and HIV disease requires accurate diagnosis.

Delayed choroidal perfusion in giant cell arteritis.

The fundus fluorescein angiograms of 13 patients with visual disturbance due to biopsy-proven giant cell arteritis (11 with anterior ischemic optic neuropathy (AION); 2 with visual obscurations only) were compared with the fluorescein angiograms from 33 patients with acute nonarteritic AION and 23 age-matched normal eyes. In all 13 patients with giant cell arteritis, the fluorescein angiograms showed a significant delay of choroidal filling time (mean 69 seconds) in comparison with either normal subjects (mean 5.8 seconds) or patients with nonarteritic AION (mean 5.5 seconds). In patients presenting with acute AION, the finding of delayed choroidal filling on fluorescein angiography should raise the index of suspicion of giant cell arteritis and lead to prompt investigation and treatment.

Influences of lesions of parietal cortex on visual spatial attention in humans.

Several brain areas have been identified with attention, because damage to these regions leads to neglect and extinction. We have tested elements of visual attentional processing in patients with parietal, frontal, or temporal lesions and compared their responses to control subjects. Normal humans respond faster in a reaction time task when the spatial location of a target is correctly predicted by an antecedent stimulus (valid cue) than when the location is incorrectly predicted (invalid cue). The cue is hypothesized to shift attention towards its location and thereby facilitate or impede response latencies. The reaction times of individuals with damage to the parietal lobe are somewhat slowed for targets ipsilateral or contralateral to the side of the lesion if the targets are preceded by valid cues. These same patients are extremely slow in responding to targets in the visual field contralateral to the lesion when the cue has just appeared in the unaffected (ipsilateral) visual field. In addition, these individuals are especially slow in responding to targets in either visual field when the lights are preceded by weak, diffuse illumination of the entire visual field. Patients with lesions of the frontal lobe have very slow reaction times in general and, as is the case for patients with lesions of the temporal lobe, are slow in all conditions for targets in the field contralateral to the lesion. These patterns are probably not associated with attentional defects. For patients with parietal lesions, these studies demonstrate a further deficit in a cued reaction-time task suggesting abnormal visual attention. Since different sites of brain damage yield different patterns of responses, tests such as these could be of analytic and diagnostic value.

Chronic syphilitic meningitis resulting in superior orbital fissure syndrome and posterior fossa gumma. A report of two cases followed for 20 years.

Two case histories, each spanning more than 20 years, demonstrate the complexity and persistence of modern neurosyphilis. Both patients present uncommon manifestations of neurosyphilis that may be easily overlooked today: superior orbital fissure syndrome, posterior fossa gumma, and bilateral deafness. Computed tomographic scans were performed in both patients but were diagnostically nonspecific, and syphilis serology testing in both serum and cerebrospinal fluid was repeatedly misleading. Numerous mistaken diagnoses were put forward until tissue was finally available for histologic examination. Perhaps the most disturbing aspects of these two cases are the persistent failure of specific treponemal serologic testing to indicate the diagnosis, and the inability of repeated "adequate" and/or supramaximal doses of penicillin to prevent continued neurologic deterioration. We believe that chronic neurosyphilis may demand a reevaluation of current diagnostic and therapeutic practice.

Optic neuropathy in chronic lymphocytic leukemia.

Ophthalmic and neurologic involvement in chronic lymphocytic leukemia is uncommon, and if it does occur, it is usually only late in the course of the disease. We report three cases in which progressive visual loss from optic nerve infiltration was an early clinical manifestation of chronic lymphocytic leukemia. Progressive optic atrophy with loss of acuity and visual field occurred in all cases, preceded in one patient by transient visual obscurations and disc edema. Surface marker studies of cerebrospinal fluid lymphocytes were useful in differentiating leukemic optic nerve infiltration from other causes of optic nerve damage. Optic nerve irradiation gave considerable clinical improvement in all three cases.

Accidental mydriasis from blue nightshade "lipstick".

A 7-year-old girl presented with bilaterally dilated pupils, nausea, and vomiting 2 days after head trauma. Pilocarpine pupil testing led to the correct diagnosis of pharmacologic pupillary dilation from an unexpected and unusual source of plant poisoning, Solanum dulcamara (blue nightshade). In patients with internal ophthalmoplegia, awareness of the possibility of pharmacologic mydriasis and correct use of topical pilocarpine testing can preclude the necessity for neuroradiologic and invasive diagnostic studies, even in cases with atypical or complex presentations.

Two cases of downbeat nystagmus and oscillopsia associated with carbamazepine.

Downbeat nystagmus is often associated with structural lesions at the craniocervical junction, but has occasionally been reported as a manifestation of metabolic imbalance or drug intoxication. We recorded the eye movements of two patients with reversible downbeat nystagmus related to carbamazepine therapy. The nystagmus of both patients resolved after reduction of the serum carbamazepine levels. Neuroradiologic investigations including magnetic resonance imaging scans in both patients showed no evidence of intracranial abnormality. In patients with downbeat nystagmus who are taking anticonvulsant medications, consideration should be given to reduction in dose before further investigation is undertaken.

The use of clonazepam in the treatment of nystagmus-induced oscillopsia.

The effect of clonazepam was studied in ten patients with nystagmus-induced oscillopsia due to downbeating or other primary position nystagmus. A 1-2-mg single-dose clonazepam test was used to determine whether long-term clonazepam therapy was indicated and to help distinguish between visual loss from underlying retinal or optic nerve disease and visual loss due to the nystagmus itself. With the single-dose clonazepam test, nystagmus was eliminated in 6 of 10 patients in the primary position of gaze and in 7 of 10 patients in downgaze. In all positions of gaze in all patients there was significant reduction in nystagmus intensity and slow phase velocity. Symptoms of oscillopsia were reduced or eliminated in all patients, and 7 of 8 patients with reduced visual acuity had clinical improvement. Guidelines are presented for the use of clonazepam in a single-dose clonazepam test and for long-term therapy.

Long-term follow-up after single toxic exposure to trichloroethylene.

In an earlier report [Feldman and Lessell, 1967], neurologic findings following acute intoxication to trichloroethylene were presented. Facial anesthesia, asymmetric pupillary responses, and electrical evidence of sensorimotor neuropathy accompanied neuropsychological deficits, manifested by difficulty in solving sequential problems and poor memory affecting the acquisition of new information. Twelve years after the initial exposure, patches of hypalgesia over the malar eminences persisted and corneal reflexes remained absent, although sensation in the snout region was totally normal. Neuropsychological test results continued to demonstrate impaired attention and short-term memory as well as diminished visuospatial organization and sequencing, 16 years after exposure. In addition, MMPI profile and interview suggested continued depressive symptomatology. Eighteen years after exposure, findings included paresthesia and hypalgesia in the malar area of the face as well as myokymia of the facial muscles. Facial nerve latency studies were normal as were pattern shift visual evoked responses. The patient continued to have large pupils that reacted asymmetrically to light. In the right eye, contraction was synchronous in all segments of the sphincter. In the left eye, there was segmental contraction, suggestive of a tonic pupil. This report offers evidence of long-term residual oculomotor and ciliary reflex dysfunction as well as impaired neuropsychological performance as a result of acute TCE intoxication.

Transient visual obscurations with elevated optic discs.

The pathogenesis of the transient obscurations of vision that occur with papilledema is a subject of speculation and debate. We present four examples of transient obscurations of vision that were clinically indistinguishable from those of papilledema; they occurred in patients with elevated optic discs from causes not related to increased intracranial pressure. The underlying mechanism for visual obscurations in all of these patients appear to be transient ischemia of the optic nerve head consequent to increased tissue pressure. Axonal swelling, intraneural masses, and increased influx of interstitial fluid may all contribute to increases in tissue pressure in the optic nerve head. The consequent reduction in perfusion pressure renders the small, low-pressure vessels that supply the optic nerve head vulnerable to compromise. Brief fluctuations in intracranial or systemic blood pressure may then result in transient loss of function in the eyes. We postulate that such mechanisms may apply in all cases of optic disc elevation, including papilledema.

A syndrome of arterial-occlusive retinopathy and encephalopathy.

An analysis of two new cases and four previously reported cases produced evidence for a syndrome of arterial-occlusive retinopathy and encephalopathy. All six patients were women; they ranged in age from 21 to 40 years. The clinical features of this condition include multiple branch retinal arterial occlusions and encephalopathy in which behavioral and memory disturbances predominate early. Hearing loss is frequent. Except for cerebrospinal fluid pleocytosis and an increased cerebrospinal fluid protein level, there are few laboratory or radiographic abnormalities. The disease may be responsive to corticosteroid therapy. There are some similarities between this syndrome and systemic lupus erythematosus but it appears to be a distinct disease entity. A comparison of the retinal findings with those described in experimental allergic encephalitis suggests that this may be a virally induced immune-mediated disease. Although only four clearly documented examples of this syndrome have been reported, we suspect that cases may have been overlooked because of failure to recognize arterial branch occlusions in the peripheral retina.

Ocular motility testing in the evaluation of visual hallucinations.

Distinguishing organic visual hallucinations from those caused by hysteria or malingering is important but difficult. We found that ocular motility testing is helpful in making the distinction in some patients who allege that their hallucinations move. A 9-year-old girl thought to have organic hallucinations, possibly caused by an occipital lobe neoplasm, was unable to generate smooth pursuit movements when she attempted to follow the movements of the hallucinations. Instead, she executed a series of small downward saccades. Her hallucinations were presumably stress-induced. Conversely, a 62-year-old man with hypertension, arteriosclerotic heart disease, and depression, whose hallucinations were thought to be hysterical, was able to execute smooth pursuit movements when he attempted to follow the hallucinations. Detection of a previously unrecognized visual field defect helped to establish that the hallucinations were organic. Thus, patients with moving organic hallucinations may produce smooth pursuit movements when attempting to follow the hallucinations, but patients with feigned or hysterical hallucinations, who lack a fixation target, are likely to execute a series of saccades.

Strokes and contraceptive medication.

PIP: 3 cases of stroke in young women of childbearing age are presented to show the severity of illness and mortality in women using oral contraceptives. All 3 patients smoked more than 15 cigarettes a day. The mortality rate from cerebrovascular disease in OC users has been estimated as 4.7 times that of nonusers. The risk of developing a thrombotic stroke is 9.5 times greater than a control group's. Cerebral infarction has a relatively low mortality rate in young women, 9%, but a nonfatal stroke can have a devastating effect on the patient and her family. While there were no deaths among the 3 cases, each was left with a varying degree of neurological deficit while still in the peak of a normal life span. The possibility of synergistic potentiation of OC-associated cerebral thrombosis by cigarette use is uncertain but studies have noted some correlation between the 2. It is not clear that reduction in estrogen dosage has reduced the risk of cardiac or cerebral disease. The first patient developed extreme symptoms after a heavy drinking session, thereby raising the question of alcohol as a precipitating factor.^ieng