Subarachnoid hemorrhage: beyond aneurysms.

OBJECTIVE: Spontaneous subarachnoid hemorrhage (SAH) typically prompts a search for an underlying ruptured saccular aneurysm, which is the most common nontraumatic cause. Depending on the clinical presentation and pattern of SAH, the differential diagnosis may include a diverse group of causes other than aneurysm rupture. CONCLUSION: For the purposes of this review, we classify SAH into three main patterns, defined by the distribution of blood on unenhanced CT: diffuse, perimesencephalic, and convexal. The epicenter of the hemorrhage further refines the differential diagnosis and guides subsequent imaging. Additionally, we review multiple clinical conditions that can simulate the appearance of SAH on CT or MRI, an imaging artifact known as pseudo-SAH.

Inferior vena cava dissection following blunt abdominal trauma.

Dissection of the inferior vena cava (IVC) is rare, with only a few published reports in the literature. It is usually associated with blunt abdominal injury or iatrogenic injury from a catheter manipulation. Venous dissections are rare due to lack of well-developed layers in the walls (intima, media and adventitia), low pressure in the venous system, and the absence of atherosclerotic changes. However, IVC dissection is associated with a high mortality rate due to the difficulty in diagnosis, technically difficult surgical repair, and associated solid organ injuries. We report a case of IVC dissection from a low-speed motor vehicle collision and discuss its imaging features.

Timing and balance of inhibition enhance the effect of long-term potentiation on cell firing.

The role of a neuron in neural processing is ultimately determined by whether or not it fires an action potential in a given context. Studies on synaptic plasticity have focused primarily on changes in EPSPs, and not on whether plasticity translates into changes in firing. However, this issue has been addressed by examining EPSP-spike (E-S) potentiation, which enhances the ability of an EPSP of a fixed slope to elicit spikes after long-term potentiation (LTP). Although LTP is thought to underlie learning and memory, E-S potentiation could play an equally important role by potentiating the neuronal input-output function. Here, we used a combined experimental and theoretical approach to examine both the mechanisms underlying E-S potentiation as well as the role of inhibition in shaping the input-output function of neurons. Whereas previous studies examined tetanus-LTP, in which inhibitory synapses may have undergone plasticity, here we examined pairing-induced associative LTP. We determined that although intact inhibition was necessary for pairing-induced E-S potentiation, inhibitory plasticity was not. We further established using computer simulations that a primary mechanism of E-S potentiation was a change in the relative recruitment and latency of inhibitory neurons. Although these studies do not exclude the presence of additional mechanisms of E-S potentiation that may be engaged depending on the induction protocol, they do establish that under intact pharmacology, LTP of the Schaffer collateral to CA1 pyramidal neuron synapses will produce E-S potentiation as a result of changes in the balance and timing of excitation and inhibition.

Differential effects of short- and long-term potentiation on cell firing in the CA1 region of the hippocampus.

Long-term potentiation (LTP) in the hippocampus enhances the ability of a stimulus to produce cell firing, not only by increasing the strength of the EPSPs, but also by increasing the efficiency of the input/output (I/O) function of pyramidal neurons. This means that EPSPs of a given size more easily elicit spikes after LTP, a process known as EPSP-spike (E-S) potentiation. In contrast to LTP, it is not known whether the synaptic strengthening produced by paired-pulse facilitation (PPF) also results in changes in the I/O function. We have addressed this question by examining E-S curves from rat hippocampal area CA1 in response to both PPF and LTP. We describe a novel form of I/O modulation in which PPF produces E-S depression; that is, the E-S curve is shifted to the right, indicating a decreased ability of EPSPs to elicit action potentials. Consistent with the notion that E-S potentiation observed with LTP is caused by long-term increases in the excitatory-inhibitory ratio, we show that PPF-induced E-S depression relies on short-term decreases in this ratio. These results indicate that different forms of synaptic plasticity that produce the same degree of EPSP potentiation can result in dramatically different effects on cell firing, because of the dynamic changes in the excitatory-inhibitory balance within local circuits.

Craniocervical hyperpneumatization with concurrent pneumorrhachis, pneumomediastinum, and subcutaneous emphysema in a weightlifter.

BACKGROUND CONTEXT: Acquired hyperpneumatization of the skull base and upper cervical vertebrae is extremely rare and is thought to occur in patients who habitually perform the Valsalva maneuver or engage in repetitive positive pressure activities such as scuba diving or free diving. Craniocervical hyperpneumatization has been reported to cause intracranial and extracranial pneumatoceles but is not generally considered as a cause of pneumorrhachis (air in the spinal canal). Pneumorrhachis is relatively rare, and usually occurs in a localized form, either in the cervical spine secondary to skull base fractures or in the thoracic spine secondary to pneumomediastinum or pneumothorax. Here, we report a case of extensive pneumorrhachis extending from the skull base to the thoracolumbar junction in association with marked axio-atlanto-occipital hyperpneumatization and pneumomediastinum. This unique constellation of findings likely resulted from complications of the Valsalva maneuver during strenuous exercise. PURPOSE: To present a unique case of axio-atlanto-occipital hyperpneumatization with concurrent marked cervicothoracic pneumorrhachis, subcutaneous emphysema, and pneumomediastinum and to provide a review of the relevant literature, pathophysiology, and treatment strategies related to hyperpneumatization and pneumorrhachis. STUDY DESIGN/SETTING: A unique case report from an urban medical center. PATIENT SAMPLE: A single case. OUTCOME MEASURES: Imaging findings and clinical history. METHODS: Imaging data from a picture archiving and communication system and clinical data from an electronic medical record system were analyzed. RESULTS: A 58-year-old previously healthy man presented with 3 to 4 weeks of neck pain, shoulder pain, and intermittent hand and finger numbness that developed after weightlifting. On physical examination, he had mild hyperreflexia and decreased pinprick sensation within the T5-T8 dermatomes. Initial radiographic and computed tomography (CT) studies demonstrated extensive craniocervical hyperpneumatization involving the occipital bone, clivus, and C1 and C2 vertebral bodies. There was also pneumorrhachis extending throughout the entire cervical and thoracic spine, which caused moderate dural compression. Pneumomediastinum and subcutaneous emphysema were present. Maxillofacial CT showed dehiscent bone involving the dens, atlas, and occipital bone, with adjacent soft-tissue gas and pneumorrhachis. He was managed conservatively and advised to stop performing the Valsalva maneuver during weightlifting. His symptoms resolved, and follow-up imaging showed complete resolution of pneumorrhachis and partial reversal of hyperpneumatization. CONCLUSIONS: Craniocervical hyperpneumatization is a rare complication of the Valsalva maneuver. Most reported cases have involved only the skull base, or the skull base and C1, and many have been further complicated by microfractures leading to pneumocephalus or extracranial pneumatoceles. We present a unique case of extensive craniocervical hyperpneumatization that extended to the level of C2 and was complicated by microfractures causing severe pneumorrhachis. Concurrent pneumomediastinum in this case may have been an independent complication of the Valsalva maneuver, which could have contributed to pneumorrhachis. Alternatively, pneumomediastinum may have been caused by migration of gas through the neural foramen from the epidural space, driven by positive pressure generated by the one-way valve effect of the Eustachian tube during periods of exertion.