Post-traumatic thoracic outlet syndrome.

BACKGROUND: To evaluate the clinical presentation, diagnostic and therapeutic management and outcome of 27 cases of post-traumatic thoracic outlet syndrome (PT TOS). METHODS: Retrospective chart analysis. RESULTS: Nineteen women and eight men were included in this study. Involvement in a traffic accident was the most common scenario. Fracture of either the first rib or the clavicle was reported in eight patients at the time of injury; in others, the diagnosis was cervical or shoulder soft tissue trauma. Upon presentation at our clinic at a mean 41 months after injury, four patients had bilateral symptoms and 17 reported decreased function of either the arm or hand. Two patients presented with severe lower trunk deficits including one who had received surgical intervention at both the cervical spine and elbow before diagnosis of TOS was made. Sixteen and 15 patients were suffering from some degree of anxiety and/or depression. Upon diagnosis of neurogenic TOS, the two patients with atrophy of the hand musculature were treated surgically. Conservative treatment was applied to all other patients. Six months after presentation to our clinic, nine patients demonstrated a significant improvement. The remainder that reported incapacitating symptoms were offered surgical treatment. Three patients declined the latter. Fifteen patients received surgical treatment via an anterior supraclavicular approach with resection of the anterior scalene muscles. Eleven patients had resection of the middle scalene muscle while five had resection of an osseous structure (partial claviculectomy, C7 transverse process or a cervical rib). The two patients with atrophy of the hand only slightly improved their motor deficit but had a notable relief of symptoms of pain. Postoperative improvement occurred in 80% of surgically treated patients. CONCLUSIONS: The majority of patients suffering from a post-traumatic TOS present a neurogenic, usually subjective syndrome. Prompt therapeutic management is necessary, addressing both physical and psychological complaints. Most patients are cured or well improved by conservative and/or surgical treatment.

Surgical management of anterior cranial base fractures with cerebrospinal fluid fistulae: a single-institution experience.

OBJECTIVE: The management of cerebrospinal fluid (CSF) fistulae after anterior cranial base fracture remains a surgical challenge. We reviewed our results in the repair of CSF fistulae complicating multiple anterior cranial base fractures via a combined intracranial extradural and intradural approach and describe a treatment algorithm derived from this experience. METHODS: We retrospectively reviewed the files of 209 patients with an anterior cranial base fracture complicated by a CSF fistula who were admitted between 1980 and 2003 to Liège State University Hospital. Among those patients, 109 had a persistent CSF leak or radiological signs of an unhealed dural tear. All underwent the same surgical procedure, with combined extradural and intradural closure of the dural tear. RESULTS: Of the 109 patients, 98 patients (90%) were cured after the first operation. Persistent postoperative CSF rhinorrhea occurred in 11 patients (10%), necessitating an early complementary surgery via a transsphenoidal approach (7 patients) or a second-look intracranial approach (4 patients). No postoperative neurological deterioration attributable to increasing frontocerebral edema occurred. During the mean follow-up period of 36 months, recurrence of CSF fistula was observed in five patients and required an additional surgical repair procedure. CONCLUSION: The closure of CSF fistulae after an anterior cranial base fracture via a combined intracranial extradural and intradural approach, which allows the visualization and repair of the entire anterior base, is safe and effective. It is essentially indicated for patients with extensive bone defects in the cranial base, multiple fractures of the ethmoid bone and the posterior wall of the frontal sinus, cranial nerve involvement, associated lesions necessitating surgery such as intracranial hematomas, and post-traumatic intracranial infection. Rhinorrhea caused by a precisely located small tear may be treated with endoscopy.

Primary central nervous system lymphoma report of 32 cases and review of the literature.

We retrospectively analyzed 32 cases of primary central nervous system lymphoma (PCNSL). Five cases were diagnosed in the period 1987-1994, for 27 cases in the period 1995-2002. There were 17 men and 15 women whose median age was 69 years. Three patients were immunodeficient. The commonest symptoms were focal deficit (16 patients) and cognitive/behaviour disturbances (14 patients). Radiologically, a total of 47 contrast-enhancing lesions were observed in 32 patients; 18 patients had deep-seated lesions. All but two patients underwent histological diagnosis following craniotomy (11 patients) and/or stereotaxic biopsy (22 patients); diagnosis was obtained on CSF cytology in one patient with a third ventricle tumour. In the last patient, the diagnosis was based on the finding of marked tumour shrinkage under corticotherapy, despite two negative histological examinations. Treatment included surgical resection (10 patients), chemotherapy (25 patients) and/or radiotherapy (12 patients). According to the therapeutic recommendations of the GELA (Groupe d'Etude des Lymphomes de l'Adulte), 19 patients received at least two courses of high-dose methotrexate; intrathecal chemotherapy was used in 20 patients with methotrexate and/or cytosine arabinoside. Radiation therapy consisted of whole brain irradiation followed by a boost on tumour site. Nine patients received a combined treatment of chemotherapy and radiotherapy. Twelve patients showed rapid progression to death. At the time of last contact, 28/32 patients (88%) had died, all from PCNSL disease or from complications due to its treatment. The median survival time was 13.9 months. We conclude that PCNSL is an increasingly frequent tumour. The diagnosis is obtained by stereotactic biopsy in the majority of cases. The prognosis appears dismal despite an intensive multidisciplinary therapeutic approach.

Acute traumatic central cord syndrome: magnetic resonance imaging and clinical observations.

OBJECT: Acute traumatic central cord syndrome has been classically thought to be caused by a hemorrhage that primarily affects the central part of the spinal cord and that destroys the axons of the inner part of the corticospinal tract devoted to the motor control of the hands. Some authors, however, have proposed that its pathogenesis is based on the destruction of the motor neurons supplying the muscles of the hand. To test the validity of these two theories, the authors retrospectively studied the magnetic resonance (MR) images obtained in 18 cases of acute traumatic central cord syndrome (ATCCS) to assess the presence of intramedullary blood and to define the distribution of the abnormal signal intensities in the cervical spinal cord. METHODS: The authors used the American Spinal Injury Association (ASIA) motor scale to assess upper- and lower-limb deficits and to evaluate its metameric distribution. The abnormal intramedullary signal was then compared with the distribution of the motor deficit. All MR imaging sessions performed in the acute stage revealed a hyperintense signal on T2-weighted sequences without any signal change suggesting the presence of intramedullary blood. The localization of this signal was distributed predominantly from the C3-4 to the C5-6 disc levels. The mean ASIA motor score was 74.3 of 100, with an unequal representation between the upper and lower limbs (32 of 50 compared with 42.3 of 50, respectively). The metameric distribution of the deficit was also unequal, with a major deficit in hand function (C8-T1) compared with the more proximal cord segments (5.2 of 10 compared with 7.8 of 10, respectively). This demonstrates the absence of any correlation between the hyperintense signal and the motor deficit distribution. CONCLUSIONS: Acute traumatic central cord syndrome cannot be explained by the injury to the gray matter at the level of motor neurons supplying the hand muscles. In agreement with recently published data, the results of this series confirm the absence of intramedullary hemorrhage and corroborate the hypothesis that ATCCS may be explained by the impairment of the corticospinal tract, which can be affected globally.