Waardenburg syndrome with anisocoria and exotropia.
(1/20)
A case of Waardenburg syndrome with unusual features such as anisocoria, exotropia is reported. (+info)
Proximal M2 false aneurysm after head trauma--Case report.
(2/20)
A 72-year-old male presented with a post-traumatic false aneurysm of the right proximal M2 artery with massive subarachnoid hemorrhage after closed head injury. Serial computed tomography (CT) and angiography showed the development of the aneurysm which was verified at autopsy. He was admitted in a drowsy state just after a motorcycle accident. Initial brain CT showed subarachnoid hemorrhage without skull fracture. Follow-up brain CT showed a huge hematoma in the right temporal lobe. He died 47 hours after the accident. Histological examination of the aneurysm showed a false aneurysm. Delayed diagnosis of traumatic aneurysms leads to high mortality, so early surgical treatment is essential to save such patients. (+info)
Late detection of supraclinoid carotid artery aneurysm after traumatic subarachnoid hemorrhage and occlusion of the ipsilateral cervical internal carotid artery.
(3/20)
BACKGROUND AND PURPOSE: We report the first case of traumatic aneurysm of the supraclinoid internal carotid artery (ICA), which we speculate may have developed or grown after traumatic occlusion of the ipsilateral cervical ICA. CASE DESCRIPTION: A 26-year-old man presented with severe traumatic subarachnoid hemorrhage (SAH) and occlusion of the right cervical ICA after a motor vehicle accident. Three-dimensional CT angiography on admission showed no aneurysm. However, cerebral angiography 3 weeks after the injury showed a large aneurysm of the right supraclinoid ICA. The aneurysm was trapped, and pathological examination showed that it was a traumatic aneurysm. CONCLUSIONS: In this case we cannot be sure that the aneurysm was not present on admission. In view of the significant SAH, a lesson of this case may be to suspect such an aneurysm early on and perform early diagnostic cerebral angiography. (+info)
Pupillary evaluation for differential diagnosis of coma.
(4/20)
OBJECTIVES: To determine the usefulness of bedside evaluation of pupils in determining the aetiology of coma by adopting a probabilistic approach. PATIENTS AND METHODS: One hundred and fifteen consecutive patients presenting with coma were enrolled in this prospective cohort during the 12 month study period in the emergency room of a community teaching hospital. Patients underwent structured clinical examinations and laboratory and imaging tests. Assignment of aetiology of coma was based on strict adherence to predetermined criteria and achieved by consensus of the two physician investigators. One year follow up was obtained in all patients. RESULTS: Aetiology of coma was determined in 98% of the patients. It was metabolic in 69 patients (60%) and structural in 46 patients (40%). Metabolic causes included drug overdose, acute alcohol intoxication, hypoglycaemia, sepsis, and pneumonia. Structural causes included intracerebral haemorrhage, subarachnoid haemorrhage, cerebral infarction, subdural haematoma, and epidural haematoma. Multivariate logistic regression analysis showed light reflex loss (likelihood ratio for positive test result 3.59) and anisocoria (likelihood ratio for positive test result 9.0) as independent predictors of structural origin. CONCLUSIONS: In this prospective study of patients presenting to the emergency room of a community based teaching hospital with coma, in about 60% the coma is of metabolic origins and in about 40% of structural origins. Light reflex loss and anisocoria suggest a structural aetiology. (+info)
The sensitivity and specificity of 0.5% apraclonidine in the diagnosis of oculosympathetic paresis.
(5/20)
AIMS: To evaluate the sensitivity and specificity of 0.5% apraclonidine test in the diagnosis of oculosympathetic paresis (OSP). METHOD: Apraclonidine (0.5%) was administered to 31 eyes, nine with a diagnosis of Horner syndrome (HS), 22 with bilateral OSP caused by diabetes, and to 54 control eyes. All were confirmed with the cocaine test. The effects on pupil diameter and upper eyelid level were observed 1 hour later. RESULTS: Apraclonidine caused a mean dilation of 2.04 mm (range 1--4.5) (p<0.001) in the pupils with OSP and it caused pupillary constriction in the control eyes with a mean change of -0.14 mm (range 0.5 to --1) (p<0.05). It caused reversal of anisocoria in all HS cases. Its effects on both pupil diameters and upper lid levels differed significantly between the groups (p<0.001). The mean elevation in the upper lid was 1.75 mm (range 1--4) in the OSP group (p<0.001) and 0.61 mm (range 0--3) in the control group (p<0.001). CONCLUSION: The effect of the apraclonidine (0.5%) test on the pupil diameter was diagnostic for OSP and had at least the same sensitivity and specificity as the cocaine test for the diagnosis of OSP. (+info)
When cluster headache was called histaminic cephalalgia (Horton's headache).
(6/20)
The Author revives his experiences and reminiscences in the frontline research and everyday clinical practice dealing with what was then called "histaminic cephalalgia" (Horton's headache). In this context, the Author, one of the historical representatives of the School of Florence, reports an outline of the contribution of this pioneering period in order to promote research ideas concerning possible brain involvement in cluster headache (CH) pathogenesis, which is currently accepted worldwide. The recent history of CH has registered remarkable progress in revealing the mystery of this pathology and it is likely that, in the near future, through the development of better education and new treatments, the overall suffering of patients will be further minimised. (+info)
Bilateral tonic pupils: Holmes Adie syndrome or generalised neuropathy?
(7/20)
AIM: To compare the pupil signs in patients with bilateral pupillotonia caused by Holmes-Adie syndrome or generalised peripheral neuropathy. METHODS: Infrared video pupillographic techniques were used to measure a number of pupil variables in patients with Holmes-Adie syndrome, generalised neuropathy (various aetiologies) and healthy age-matched control subjects. RESULTS: Regardless of aetiology, the patients generally had pupil signs typical of pupillotonia (small dark diameters, large light diameters, tonic near responses, attenuated light responses with light-near dissociation, and sector palsy). However, significant differences were found in the prevalence and magnitude of several pupil variables in the two patient groups. In particular, sector palsy and anisocoria exceeding 1 mm (in the light) were seen much more commonly in Holmes-Adie patients than patients with generalised neuropathy. The presence of both these pupil signs can be used to distinguish between these diagnoses with a sensitivity of 58% and a specificity of 90%. CONCLUSIONS: The tonic pupils of patients with Holmes-Adie syndrome are significantly different to those found in patients with generalised neuropathy; recognition of these differences may allow distinction between these diagnoses. (+info)
Sex-specific lateralization of contraction anisocoria in transient pupillary light reflex.
(8/20)