Background We describe a patient with tardy ulnar neuropathy and cubitus valgus deformity found to have an intracapsular ulnar nerve. Methods An 89-year-old woman presented with severe neuropathic pain in the ulnar digits of the hand, advanced degenerative arthritis of the elbow, and tardy ulnar nerve palsy. Her pain was exacerbated with elbow movement, particularly flexion. She had paralysis of ulnar nerve innervated muscles, hypersensitivity with absence of two-point discrimination in her ulnar 1–1/2 digits, and a fixed ulnar claw deformity. She also had a grossly unstable elbow. Results Plain films revealed a cubitus valgus deformity (38°), an absent radial head, a dislocated proximal radioulnar joint and advanced arthritic changes. Ultrasonography revealed an indistinct ulnar nerve within the cubital tunnel which penetrated the joint. Electrophysiological studies revealed evidence of a severe ulnar neuropathy at the level of the elbow. Intraoperatively, an attenuated 2 cm length of the retrocondylar ulnar nerve was observed to be incorporated into the joint capsule tethered by a fibrous/synovial band which was released. A large effusion was drained. The ulnar nerve was transposed subcutaneously. The capsular rent was repaired in layers. She noted immediate and sustained (2 year follow-up) pain relief and regained moderate function in her interossei. Conclusions We believe that the chronic cubitus valgus deformity and secondary degenerative elbow joint changes led to an altered course of the nerve and attenuation of the medial joint capsule such that the ulnar nerve spontaneously buttonholed itself intra-articularly.
Misdirection of regenerating axons is one of the factors that can explain the limited results often found after nerve injury and repair. In the repair of mixed nerves innervating different distal targets (skin and muscle), misdirection may, for example, lead to motor axons projecting toward skin, and vice versa—that is, sensory axons projecting toward muscle. In the repair of motor nerves innervating different distal targets, misdirection may result in reinnervation of the wrong target muscle, which might function antagonistically. In sensory nerve repair, misdirection might give an increased perceptual territory. After median nerve repair, for example, this might lead to a dysfunctional hand. Different factors may be involved in the misdirection of regenerating axons, and there may be various mechanisms that can later correct for misdirection. In this review the authors discuss these different factors and mechanisms that act along the pathway of the regenerating axon. The authors review recently developed evaluation methods that can be used to investigate the accuracy of regeneration after nerve injury and repair (including the use of transgenic fluorescent mice, retrograde tracing techniques, and motion analysis). In addition, the authors discuss new strategies that can improve in vivo guidance of regenerating axons (including physical guidance with multichannel nerve tubes and biological guidance accomplished using gene therapy).
Object Patients with brachial plexus injury (BPI) present with a combination of motor weakness/paralysis, sensory deficits, and pain. Brachial plexus injury is generally not believed to be associated with headaches. However, CSF leaks may be associated with CSF volume–depletion (low-pressure) headaches and can occur in BPI secondary to nerve root avulsion. Only a few cases of headaches associated with BPI have been reported. It is unknown if headaches in patients with BPI occur so rarely, or if they are just unrecognized by physicians and/or patients in which the focus of attention is the affected limb. The aim of this study was to determine the prevalence of CSF volume–depletion headaches in patients with BPI. Methods All adult patients presenting at the Mayo brachial plexus clinic with traumatic BPI were asked to complete a questionnaire addressing the presence and quality of headaches following their injury. The patients' clinical, injury, and imaging characteristics were subsequently reviewed. Results Between December 2008 and July 2010, 145 patients completed the questionnaire. Twenty-two patients reported new onset headaches occurring after their BPI. Eight of these patients experienced positional headaches, suggestive of CSF volume depletion. One of the patients with orthostatic headaches was excluded because the headaches immediately followed a lumbar puncture for a myelogram. Six of the other 7 patients with positional headaches had a clear preganglionic BPI. The available imaging studies in these 6 patients revealed evidence of CSF leaks: pseudomeningoceles (n = 5), CSF tracking into soft tissues (n = 3), CSF tracking into the intraspinal compartment (n = 3), CSF tracking into the pleural space (n = 2), and low-positioned cerebellar tonsils (n = 2). Conclusions In this retrospective study, 15.2% of patients (22 of 145 patients) with traumatic BPI suffered from a new-onset headache. Seven of these patients (4.8%) experienced postural headaches clearly suggestive of CSF volume depletion likely secondary to a CSF leak associated with the BPI, whereas the other 15 patients (10.3%) suffered headaches that may have represented a variant of CSF depletion headaches without a postural characteristic or a headache from another cause. These data suggest that CSF volume–depletion headaches occur in a significant proportion of patients with BPI and have been underrecognized and underreported.