MRI detection of cerebral lesions in post-traumatic anisocoria: specificity and prognostic significance.

AIM: To identify whether increased numbers of brainstem lesions are found in the presence of a post-traumatic pupillary function disturbance and classify them anatomically. MATERIALS AND METHODS: In this study, a diagnostic magnetic resonance imaging (MRI) examination was performed within 8 days after traumatic brain injury (TBI) in patients who had been unconscious for more than 24 hours post-TBI. The Glasgow Outcome Scale was evaluated 6 months after TBI. The data obtained from 140 consecutively enrolled patients between 2005 and 2011 were analysed. The clinical study parameter comprised the development of post-traumatic anisocoria at least once over the course between onset of trauma and diagnostic MRI, as a yes/no decision. Significance was presumed at p≤0.05. RESULTS: A total of 57 patients (41%) were found to have a lesion at MRI without involvement of the brainstem; in 83 (59%) the brainstem was (multiple) affected. Of the latter, 66 (46%) of patients had lesions in the midbrain, 38 (27%) in the pons, and seven (5%) in the medulla oblongata. By the time of MRI, anisocoria had been diagnosed in 45 (32%) patients. Mortality was highest, at 58%, in patients with anisocoria and a midbrain lesion, whilst it was 23% in those with anisocoria and no lesion in the midbrain. Mortality was 33% in relation to a midbrain lesion without anisocoria. CONCLUSION: Overall, the study demonstrated that there is a significant correlation between midbrain lesions and post-traumatic anisocoria in unconscious trauma patients. A brainstem lesion in this case can be assumed to be a pathomorphological correlate of anisocoria. The rate of damage to the midbrain was approximately 50% in cases of transient anisocoria. It can be assumed in this situation that there are functional disorders of the peripheral oculomotor nerve or identifiable/unidentifiable lesions of the brainstem.

An approach to anisocoria.

PURPOSE OF REVIEW: Anisocoria is a finding seen on a daily basis in nearly every eye clinic. Although often benign, it can also represent the sole sign of a life-threatening disease making an up-to-date understanding of pathophysiology and diagnosis essential for anyone practicing medicine. RECENT FINDINGS: Many aspects of the traditional approach to anisocoria still hold true today, but advancements in imaging technology and changing trends in pharmacologic diagnosis and localization have led many to rethink that approach. In addition, the differential diagnosis for anisocoria continuously expands with identification and improved understanding of causal disease processes. SUMMARY: The present article discusses an approach to the classic anisocoria diagnostic algorithm modified by current knowledge from the most recent literature.

Ultra-early aneurysmal rebleeding and brainstem destruction.

BACKGROUND: Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, parenchymal hematoma, or seizures. METHODS: Case report. RESULTS: A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem parenchyma and ventricles. CONCLUSIONS: Sudden clinical deterioration after SAH with coma and a fixed "blown" pupil may result from hemorrhage extension into the brainstem parenchyma rather than oculomotor nerve injury from compression or stretch.

Monitoring intracranial pressure in patients with malignant middle cerebral artery infarction: is it useful?

OBJECT: Intracranial pressure (ICP) monitoring is increasingly used in the treatment of patients with malignant middle cerebral artery (MCA) infarction. However, neurological deterioration may exist independent from intracranial hypertension. This study aimed to present the findings of continuous ICP monitoring in a cohort of patients with malignant MCA infarction and to correlate these findings with clinical and radiological features. METHODS: The authors studied a prospective cohort of 25 patients with malignant MCA infarction consecutively admitted to the neurotrauma intensive care unit of the Vall d'Hebron University Hospital between March 2002 and September 2006. The patients were treated using a combined protocol of initial moderate hypothermia and hemicraniectomy. The latter was performed when patients showed a midline shift (MLS) > or = 5 mm or ICP > 20 mm Hg. Six patients had an MLS > or = 5 mm on the first CT scan and underwent surgery without prior ICP monitoring. This study focuses on the subgroup of 19 patients who underwent intraparenchymatous ICP monitoring before surgery. RESULTS: Intracranial pressure readings were evaluated and correlated with pupillary abnormalities, MLS, and ischemic tissue volume. In 12 of the 19 patients, ICP values were always < or = 20 mm Hg, despite a mean (+/- SD) MLS of 6.7 +/- 2 mm and a mean ischemic tissue volume of 241.3 +/- 83 cm(3). In 2 patients with anisocoria, ICP values were also normal. CONCLUSIONS: In patients with a malignant MCA infarction, pupillary abnormalities and severe brainstem compression may be present despite normal ICP values. Therefore, continuous ICP monitoring cannot substitute for close clinical and radiological follow-up in the management of these patients.

Computed tomographic angiography for the diagnosis of blunt carotid/vertebral artery injury: a note of caution.

OBJECTIVE: Computed tomographic angiography (CTA) by 16-channel multidetector scanner is increasingly replacing conventional digital subtraction angiography (DSA) for diagnosing or excluding blunt carotid/vertebral injuries (BCVI). To date there has been only 1 study in which all patients received both examinations. That study reported a high accuracy for 16-detector CTA. The current prospective parallel comparative study aims at validating this high accuracy and examining the rates of evaluability of CTA performed with a 16-detector scanner with image reconstruction by modern imaging software. METHODS: Patients at risk for BCVI (facial/cervical-spinal fractures; unexplained neurologic deficit; anisocoria; lateral neck soft tissue injury; clinical suspicion) underwent both CTA (16-channel multidetector scanner) and DSA. Results of the 2 studies and the clinical course were prospectively recorded. RESULTS: During the 40-month study period ending March 2007, approximately 7000 blunt trauma patients were evaluated and of these 119 (1.7%) consecutive patients meeting inclusion criteria were screened by CTA. Ninety-two patients underwent confirmatory DSA. Twenty-three (22%) DSA identified 26 BCVI (vertebral, 13; carotid, 13). Among these 23 CTAs, 17 identified 19 BCVIs (vertebral, 10; carotid, 9) (true positives), and 6 failed to identify 7 BCVIs (vertebral, 3; carotid, 4) (false negatives). Sixty-nine of the 92 DSA were normal. Of these 69 CTAs, 10 were falsely suspicious for 11 BCVIs (vertebral, 7; carotid, 4) (false positives), and 56 were normal (true negatives). The remaining 3 CTAs were nonevaluable (mistimed contrast, 1; streak artifact, 2). Sixteen of 89 (18%) evaluable CTAs, were suboptimal (mistimed contrast, 9; streak artifacts, 4; motion artifact, 2; body habitus, 1). Excluding the 3 nonevaluable CTAs, the sensitivity, specificity, positive and negative predictive values of CTA for diagnosing or excluding BCVI were 74%, 86%, 65%, and 90% respectively. One patient with grade II carotid artery injuries (by CTA and DSA) on antiplatelet agent developed stroke related to carotid artery injuries. CONCLUSIONS: Current CTA technology cannot reliably diagnose or exclude BCVI. Twenty percent of CTAs are either nonevaluable or suboptimal. Until more data are available and the technique is standardized, the current trend towards using CTA to screen for and/or diagnose these rare but potentially devastating injuries is dangerous.

[Horner's syndrome after fracture of the first rib]. / Horner-Syndrom nach Fraktur der ersten Rippe.

Horner's syndrome after trauma is rare. After visual diagnosis, a search for the cause is urgent due to possible life threatening damage. Intracerebral bleeding and carotid dissection must be excluded. Traumatic Horner's syndrome often seems to be, as in the case described here, caused by a fracture of the first rib. As persistent symptoms are not described, conservative therapy is recommended.