Kinked again! From congenital brachial plexus palsy to adult neurogenic thoracic outlet syndrome: Case Report.

ABSTRACT: Neurogenic thoracic outlet syndrome (nTOS) is a chronic, focal lesion of the lower trunk of the brachial plexus or of the T1 and C8 anterior primary rami, often arising due to distortion of neural structures by a fibrous congenital band extending from a C7 transverse process or cervical rib. Accordingly, patients present with chronic weakness or atrophy of the hand, most prominently of the thenar eminence, which receives most innervation from the T1 root. We present clinical, electrophysiologic, and imaging findings in a case of nTOS presenting in an adult with a history most suggestive of congenital brachial plexus palsy (CBPP), another pathology sharing the mechanism of nerve compression or injury within the supracostoclavicular space. The patient had new right thenar eminence atrophy and a lifelong history of medial forearm sensory deficit and she improved after first rib resection. The convergence of two disorders in the same patient arising in different phases of life illustrates how anatomic or structural variation in this space can predispose to lower brachial plexus injury.

Horner syndrome due to right subclavian artery dissection: Case report.

This is a novel case of spontaneous subclavian artery dissection presenting with an asymptomatic right Horner Syndrome, highlighting both the importance of carefully evaluating the pupils on comprehensive exam, and also the subclavian arteries when assessing for the cause of Horner Syndrome. This original case serves as a caution for practitioners not to overlook the subclavian arteries in the search for the cause of Horner Syndrome. While rare, spontaneous subclavian artery dissection can occur, and carries a risk of morbidity and mortality that must be mitigated. We present a case of asymptomatic, atraumatic right Horner Syndrome where a spontaneous right subclavian artery dissection was found to be the source. It was managed with aspirin therapy and the patient has not suffered any subsequent cardiovascular events related to the dissection. Careful angiographic evaluation of the subclavian arteries should be included in the workup for Horner Syndrome to assess for subclavian artery dissection.

Acute Isolated Sixth Nerve Palsy Caused by Unruptured Intradural Saccular Aneurysm.

BACKGROUND: Unruptured intracranial aneurysms that cause isolated sixth nerve palsies are usually located extradurally in the cavernous sinus or intradurally as part of fusiform enlargement of the parent artery. Intradural saccular aneurysms of the vertebrobasilar circulation are a rare but life-threatening cause of isolated sixth nerve palsy. We provide documentation of 2 such cases. METHODS: Case records of the Neuro-ophthalmology Clinics at the University of Michigan. RESULTS: A 56-year-old woman with an arteriosclerotic risk profile reported new diplopia and had an isolated left sixth nerve palsy caused by an unruptured saccular aneurysm of the anterior inferior cerebellar artery. It was successfully coiled, and the sixth nerve palsy markedly improved. A 62-year-old woman with an arteriosclerotic risk profile and new diplopia had an isolated right sixth nerve palsy caused by a large unruptured vertebral artery aneurysm. It was coiled and later stented and recoiled. These procedures isolated the aneurysm and relieved the sixth nerve palsy. CONCLUSIONS: Isolated sixth nerve palsies in these 2 older adult patients with arteriosclerotic risk profiles were caused by unruptured intradural vertebrobasilar aneurysms. This report adds documentation to a rare phenomenon that must be taken into consideration in deciding whether brain imaging is needed in isolated sixth nerve palsy.

Radiation-Induced Optic Neuropathy: Clinical and Imaging Profile of Twelve Patients.

BACKGROUND: Radiation-induced optic neuropathy (RON) is a form of delayed radionecrosis of the anterior visual pathways, which develops within months to years after external cranial irradiation and causes severe and irreversible vision loss. Small series reports have adequately documented its clinical features, but imaging characteristics have been less completely described. METHODS: We accrued cases from the University of Michigan Neuro-Ophthalmology Clinic files and from cases coded as "radiation optic neuropathy" at the University of Michigan Medical Center between 1994 and 2017. All patients had undergone 3D-conformal linear accelerator (photon) external beam radiation. We collected clinical details of vision loss, including the temporal relationship to radiation. A single neuroradiologist (E.A.L.) evaluated all available magnetic resonance imaging (MRI) studies, noting the presence of enhancement, expansion, or volume loss of the optic nerves or chiasm, corresponding T2 signal abnormalities, and the absence of demyelination or confounding compressive lesions. RESULTS: Twelve patients (15 eyes) met inclusion criteria. Vision loss was usually monocular at outset, but both optic nerves were eventually involved in 3 (25%) patients. Although usually sudden in onset, vision loss often declined slowly over many months, frequently to finger counting, or worse without recovery. An afferent pupillary defect was always present at the time of presentation. Most affected optic discs were pale at the time of first visual symptoms, indicating that subclinical optic nerve damage had been present for several weeks. The latency from completion of radiation to onset of vision loss ranged from 7 to 48 months (average: 18 months). In 2 patients, radiation was delivered to the whole brain, rather than being limited to the anterior visual pathway. MRI typically displayed a discrete region of enhancement of the affected prechiasmatic optic nerve, often with expansion and high T2 signal in the enhancing segment. In 3 affected eyes, enhancement was apparent on imaging completed 3-6 weeks before the onset of vision loss. In one patient, segmental prechiasmatic enhancement became evident only on repeat MRI completed 7 months after vision loss. The duration of enhancement among 9 eyes with follow-up MRIs was at least 2 months, but in one case, enhancement was still present on a study performed 17 months after treatment. CONCLUSIONS: This study further delineates the profile of RON. Visual loss is often acute, profound, and monocular but may decline slowly after acute onset and later affect both optic nerves. High-resolution MRI of the optic nerves usually will display enhancement of a discrete segment of the intracranial prechiasmatic optic nerve, often with accompanying expansion and T2 hyperintensity. In some cases, these imaging features may precede vision loss. They may be subtle or appear after vision loss. Enhancement lingers for a wide interval, ranging in this study from 2 to at least 17 months. Recognition of these imaging characteristics assists in confirmation of the diagnosis of RON.

Extra Z-axis coverage at CT imaging resulting in excess radiation dose: frequency, degree, and contributory factors.

OBJECTIVE: To assess the degree of extra scanning beyond the prescribed anatomic boundaries for thoracic and body computed tomographic (CT) scans and to identify associated factors. METHODS: For 442 consecutive chest, abdomen, and/or pelvis CT examinations, the length of extra scanning beyond the prescribed anatomic boundaries was determined. Examinations were grouped according to the locations/types of the prescribed boundaries and compared with regard to length of extra scanning. RESULTS: Of 442 CT examinations, 438 (99%) included extraneous imaging, showing a mean excess scanning length of 43.2 mm per examination (range, 0-180 mm). Significantly more extraneous imaging was performed when soft tissue or vascular structures defined anatomic boundaries compared to when osseous (P < 0.001) or air/soft tissue interfaces (P < 0.0001) defined the boundaries. The average percent of total scan dose attributable to extra imaging was 8.64% to 10.38%. CONCLUSIONS: Computed tomographic scanning beyond the prescribed anatomic boundaries occurs commonly, resulting in moderate extra radiation dose.