Neurogenic thoracic outlet associated with carpal tunnel syndrome: is this a clinical example of double crush hypothesis?

The aim of this study was to assess the possible contribution of the double crush hypothesis [DCH] for the association of carpal tunnel syndrome [CTS] with neurogenic thoracic outlet syndrome [NTOS]which -if confirmed- can explain some of the not uncommonly persistent CTS cases despite being confirmed and properly treated, particularly that NTOS is potentially treatable. 137 CTS patients [91 [66.4%] females, 46[33.6%] males], with mean age 39.4, ranging from 23 to 48 years, were included in the study based solely on electrophysiological criteria of CTS [distal motor latency to abductor pollicis brevis > 4 ms, 3 rd digit to wrist orthodromic sensory conduction velocity < 45m/s, or orthodromic median/ulnar latency difference of the 4[th] digit > 0.4 ms]. Patients who proved suffering peripheral neuropathy or entrapment of ulnar nerve were excluded. Twenty apparently healthy individuals, age and sex matched with patients were included as a control group. The patients and control groups were subjected to clinical neurological evaluation. Electrophysiological work up including motor/sensory conduction study of median and ulnar nerves on both sides, and bilateral medial antebrachial cutaneous nerve [MABCN] antidromic sensory, considering side to side MABCN sensory nerve action potentials [MABCN SNAP] amplitude ratio of >2.0 as abnormal. Electrophysiological criteria used for confirming [NTOS], were low median compound motor action potentials [CMAP], low ulnar SNAP, low or normal ulnar CMAP, normal or reduced interference pattern of C8 T1-innervated muscles, and MABCN SNAP interside amplitude ratio >2.0[the latter was used as a mandatory inclusion criterion]. Patients with atypical upper limb pain have undertaken cervical plain X ray. Control group was subjected to complete neurophysiological studies. Student t test was used to compare means of two groups. Ulnar nerve SNAP amplitudes were found normal. Reduction of median CMAP was reported in 19 patients [13.86%] and it was bilateral in 7 [36.84%]. Antidromic MABCN SNAP interside amplitude ratios showed values <2.0 and mean +/- SD was 1.273 +/- 0.221. Needle examination showed incomplete interference pattern in abductor pollicis brevis muscles in 11 patients [8%]. 3 patients [5.26%], 2 males, and 1 female had bilateral bony cervical ribs but non had evidence of NTOS. Neurophysiologically confirmed CTS was not proved to associate NTOS, and the hypothesized relationship between them could not be obtained. This might inspire us to revisit DCH for re-evaluation. Finally, NTOS is still a rare medical condition and scrutinizing suspected cases with thorough clinical assessment, and electrophysiological work up is a must

Study of the occurrence of abnormal involuntary movements after cerebral stroke

Abnormal involuntary movements [AIM] following cerebral stroke were reported after lesions in certain areas of the brain, but most of these studies were case reports or series of patients with a given type of abnormal movement or anatomical lesion. The aim is to study pattern of occurrence of AIM that may occur after cerebral stroke and their relationship to the cause of stroke, clinical and personal data of patients as well as sites of lesions based on imaging studies. Thirty four patients with AIM after cerebral strokes were included in this study. These patients were selected suffering first ever clinical stroke, with negative history of previous attacks. These patients were subjected to medical history taking, and thorough neurological examination. The type of AIM was evaluated by more than one of the authors separately with consultation of every case. Clinical follow up of these AIM was done using abnormal involuntary movements scale [AIMS] for detection of improvement or deterioration of these abnormal movements. Also clinical follow up of the motor power, sensory deficits, cerebellar manifestations etc was done. Follow up was done every two weeks in the first month and every month afterward and patients were followed up for at least a year after onset of AIM. Patients that died or did not comply with the study were excluded, also patients with previous history of AIM before onset of stroke were excluded as well. All patients were subjected to CT brain in the acute stage of stroke and those that had normal CT in the acute stage were resubjected to CT or MRI brain. Another 3 cases of central thalamic ischemic lesions, authors came across while doing this research, were included and studied as previously. Thirteen [38.2%] of patients suffered chorea, while only 4 [11.7%] suffered parkinsonism and patients with tremor and dystonia were 9 [26.4%], and 8 [23.5%] respectively. Group of patients with chorea were found significantly [P<0.05] the elder among the other groups. The shortest mean interval time between onset of stroke and development of AIM was that for chorea with statistical significant difference [P<0.05]. Most of the patients with AIM were grade 4 and 5 on MRC scale, and of moderate to severe affection of proprioceptive sensation and ataxia. Although lesions of the thalamus and/or basal ganglia were found common in these patients, good percent of patients were found suffering lesions in other areas of the brain. Central thalamic lesion was accompanied with contralateral hypothesis, chorea, and ataxia. Correlation between site of lesion and type of AIM could be difficult to establish. Although thalamic and basal ganglion lesions are common underlying cause for AIM, these AIM could occur in a good percentage after lesions in other areas of the brain and that could be due to concurrent ataxia and proprioceptive sensory impairment beside reasonable motor strength. Finally, pathogenesis of AIM needs more speculation and more scrutinized analysis of imaging studies with paying more attention to functional brain imaging studies