Case report: Liposarcoma of the sinonasal tract.

Nasal and paranasal malignant tumours account for less than 5% of all head and neck malignancies. Epithelial malignancies overwhelmingly predominate, with squamous cell carcinomas representing the most frequent histological subtype in this location. Soft-tissue sarcomas of the nasal cavity and paranasal sinuses are exceedingly rare. Here, we report two cases of myxoid liposarcomas that occurred in the nasal and paranasal regions, both of which presented diagnostic challenges and could not be diagnosed definitively from intraoperative frozen sections. These cases reinforce the notion that, while they are uncommon, sarcomas in general and liposarcomas in particular should still be considered as part of the differential diagnosis in patients presenting with obstructive symptoms in the nasal and paranasal sinuses.

Diagnosis and treatment of thoracic outlet syndrome.

TOS represents a spectrum of disorders encompassing four related syndromes: arterial compression, venous compression, neurogenic compression, and a poorly defined pain syndrome. Patients can present with signs of arterial insufficiency, venous obstruction, painless wasting of intrinsic hand muscles, and pain. History and physical examination are the most important diagnostic studies, and radiographs of the chest and cervical spine and electromyography/nerve conduction studies are useful to identify other causes of pain and disability. Surgical intervention is indicated for patients failing nonoperative maneuvers and can usually yield satisfactory results. TOS may also be the most underrated, overlooked, and misdiagnosed, and the most important and difficult to manage peripheral nerve compression in the upper extremity.

Nerve injury-induced mechanical but not thermal hyperalgesia is attenuated in neurokinin-1 receptor knockout mice.

Mice lacking the gene encoding for substance P and neurokinin A, or the NK-1 receptor, exhibit alterations in behavior to various acute nociceptive stimuli. However, behavioral responses of NK-1 mutant animals have not been well characterized in models of chronic pain. We studied the behavioral responses of NK-1 knockout and wild-type control mice to thermal and mechanical stimuli before and after inducing chronic neuropathic pain by unilateral ligation of the L5 spinal nerve. Mechanical hyperalgesia was evaluated by determining the frequency of withdrawal to von Frey monofilaments applied to the hind paws. Nerve injury-induced hyperalgesia to thermal stimuli was examined by determining responses to radiant heat and cooling stimuli. The contribution of the sympathetic nervous system to mechanical hyperalgesia was evaluated by administering 3 mg/kg phentolamine, an alpha-adrenergic antagonist, subcutaneously. Following spinal nerve injury, withdrawal frequencies to mechanical stimulation increased in wild-type mice within 1 day and persisted during the 9-week observation period, whereas in the knockout mice, withdrawal frequencies did not increase significantly. In contrast, withdrawal latencies to radiant heat decreased up to 2 weeks after nerve injury in both the NK-1 and the wild-type mice. Similarly, the increase in withdrawal frequency to the cooling stimuli following the nerve injury was not different in the NK-1 knockout and wild-type mice. Mechanical hyperalgesia in the wild-type mice was not reversed by systemic administration of phentolamine, suggesting that the pain is not sympathetically maintained. The results indicate that NK-1 receptors contribute to the development of mechanical, but not thermal, hyperalgesia in neuropathic pain.

Cerebrovascular reserve capacity many years after vasospasm due to aneurysmal subarachnoid hemorrhage. A transcranial Doppler study with acetazolamide test.

BACKGROUND AND PURPOSE: Vasospasm in aneurysmal subarachnoid hemorrhage results in proliferative vasculopathy. Systemic hypertension also causes vascular hypertrophy. Both of these histological changes can lead to rigidity of the cerebrovascular system, reducing its autoregulatory capacity. METHODS: Blood flow velocity (BFV) in the middle cerebral artery at rest and cerebrovascular reserve capacity (CVRC) (percent rise in BFV after acetazolamide stimulation) measured by means of transcranial Doppler sonography were studied many years after aneurysmal subarachnoid hemorrhage in patients with proven cerebral vasospasm (mean BFV > 160 cm/s). The BFV under resting conditions and the CVRC values of the ipsilateral and the contralateral hemispheres were measured in 29 patients (mean age, 43 years; mean follow-up, 4.6 years) and compared with those of control subjects. RESULTS: Persistent high BFV (> 120 cm/s) was found in three patients in the peripheral branch of the ipsilateral middle cerebral artery. In the main trunks of the arteries of the anterior circle of Willis, BFV was normal in all cases. CVRC was normal in all patients (ipsilateral, 52 +/- 21%; contralateral, 56 +/- 17%); values did not differ significantly from each other or from the control value (45 +/- 18%). The higher value of CVRC on the contralateral side was found to be statistically significant in selected groups (hypertensive patients and patients with residual infarct on late CT). CONCLUSIONS: Proliferative vasculopathy developed at the time of vasospasm must have resolved and did not reduce late vasoreactivity. Comorbidity with hypertension also did not seem to influence the late vasoreactivity toward normalization.