Faculty Bibliography

An entrapment syndrome is defined as a chronic nerve irritation in fibro-osseous tunnel. The entrapment syndromes of the lower extremities ore the following. 1.) tarsaltunnel syndrome with compression of the tibial nerve posterior and inferior to the medial malleolus, 2.) Morton's syndrome with irritation of the 4(th) N. digitalis plantaris communis between the capitula of the 3(rd) and 4(th) metatarsal bones, 3.) saphenus neuropathy with compression of the saphenus nerve in the canalis adductorius Hunter, 4.) meralgia paraesthetica with irritation of the lateral cutaneaus nerve beneath the inguinal ligament, 5.) piriformis syndrome with compression of the sciatic nerve under the piriformis muscle, 6.) ilioinguinalis syndrome with lesion of this nerve passing the muscles of the abdominal well. The diagnosis con partially be ensured by electrodiagnostic methods. Therapeutically, infiltrations of local anaesthetic drugs can be performed or surgical exploration and decompression will be necessary. $$:

In 225 adults aged 18 to 80 years, normative warm and cold perception thresholds were assessed at the volar distal forearm, thenar eminence, lower medial calf, and lateral dorsal foot using the method of limits and a Thermotest (Somedic, Stockholm, Sweden). A 1.5-cm x 2.5-cm thermode, a 1 degrees C/s stimulus change rate, and a 32 degrees C baseline temperature were applied. Thresholds of five consecutive stimuli were averaged. At the thenar eminence a 3 degrees C/s stimulation was applied in addition to the 1 degree C/s stimulation. Effects of spatial summation were studied at the calf and forearm by additional testing with a 2.5-cm x 5.0-cm thermode. To evaluate the influence of skin temperature, thresholds were correlated with the pretest skin temperature at the tested sites. Reproducibility of stimulus perception was determined by comparing the lowest to the highest response to five consecutive stimuli. Results showed sufficient accuracy of thermal perception thresholds. Thresholds were higher with the 3 degrees C/s stimulation than with the 1 degree C/s stimulation. Thresholds were lower with the large than with the small probe. Skin temperature had only minimal influence on thresholds. The use of a 32 degrees C baseline temperature and a 1 degree C/s stimulus change rate is recommended. The large probe should be used at body sites where the entire thermode surface adjusts planely to the skin. Warming up the tested skin area is not necessary before thermotesting

To determine whether sympathetic skin response (SSR) testing evaluates afferent small or efferent sympathetic nerve fiber dysfunction, we studied SSR in patients with familial dysautonomia (FD) in whom both afferent small and efferent sympathetic fibers are largely reduced. We analyzed whether the response pattern to a combination of stimuli specific for large or small fiber activation allows differentiation between afferent and efferent small fiber dysfunction. In 52 volunteers and 13 FD patients, SSR was studied at palms and soles after warm, cold and heat as well as electrical, acoustic, and inspiratory gasp stimulation. In addition, thermal thresholds were assessed at four body sites using a Thermotest device (Somedic; Stockholm, Sweden). In volunteers, any stimulus induced reproducible SSRs. Only cold failed to evoke SSR in two volunteers. In all FD patients, electrical SSR was present, but amplitudes were reduced. Five patients had no acoustic SSR, four had no inspiratory SSR. Thermal SSR was absent in 10 patients with abnormal thermal perception and present in one patient with preserved thermal sensation. In two patients, thermal SSR was present only when skin areas with preserved temperature perception were stimulated. In patients with FD, preserved electrical SSR demonstrated the overall integrity of the SSR reflex but amplitude reduction suggested impaired sudomotor activation. SSR responses were dependent on the perception of the stimulus. In the presence of preserved electrical SSR, absent thermal SSR reflects afferent small fiber dysfunction. A combination of SSR stimulus types allows differentiation between afferent small or efferent sympathetic nerve fiber dysfunction

BACKGROUND: The prevalence of patent foramen ovale (PFO) in healthy individuals is estimated to be about 25% and is elevated to 40% patients with stroke. To date transesophageal echocardiography (TEE) was considered to be the most sensitive method to detect PFO and was regarded as the gold standard. Transcranial Doppler sonography of the middle cerebral artery during contrast injection (c-TCD) has recently been proposed as an alternative method for the detection of PFO. We report our experience on 45 patients (age < 55 years) with stroke or transient ischemic attack (TIA) in whom both c-TCD and TEE were performed to detect PFO as a mechanism for embolic cerebral ischemia. PATIENTS AND METHODS: In 45 patients (21 women, 24 men, mean age 41.4 years ranging from 17 to 54 years) with cerebral ischemia, both standardized TEE and standardized c-TCD were performed separately. When any PFO was found by TEE and/or c-TCD, it was classified as positive. If c-TCD was positive but TEE negative, a second TEE was performed and vice versa. RESULTS: PFO was found epicritically in 26 patients (57.8%). First TEE detected PFO in 24 cases (sensitivity 92.3%). Separately performed c-TCD detected PFO in 22 cases of the PFO-positive cases (sensitivity 84.6%). However, c-TCD detected PFO in 2 cases, in which the first TEE had been negative, leading to a second TEE which confirmed PFO and demonstrated minimal shunt (7.7%). TEE detected PFO in 4 cases in which first c-TCD was negative. A second c-TCD confirmed in 2 of these 4 cases a positive right-to-left shunt. Neither method revealed false positive results (specifity 100%). The positive predictive value was 100% in both methods. The negative predictive value in TEE was 90.5% and in c-TCD was 82.6%. CONCLUSION: TEE and c-TCD are not concurrent diagnostic tools to detect PFO. Both supplement each other. If both methods are used in all PFO-suspected patients, PFO detection rate is higher than when using either method alone

Cerebrovascular hemodynamics during postural changes have been sparsely investigated despite the fact that abnormal responses may contribute to the risk of stroke. The aim of this study was to determine the effect of acute 80 degrees head-down tilt (HDT) on cerebrovascular hemodynamics in humans using transcranial Doppler sonography (TCD). In 13 healthy volunteers (2 female, 11 male, age 19-37 years, mean age 26.8 years) left midcerebral artery blood flow velocities (CBFVs) were continuously monitored using TCD during 180 sec in horizontal position and during 60 sec of 80 degrees HDT. Simultaneously, systolic, diastolic, mean CBFVs, pulsatility index (PI), heart rate, beat-to-beat blood pressure (BP) and transcutaneous pCO2 were measured. In five volunteers, the procedure was repeated the next day to test the repeatability of the results. Mean BP increased slightly, but not significantly during tilt (from 80.5 +/- 7.7 mmHg to 85.9 +/- 14.1 mmHg; p > 0.05). Heart rate decreased significantly during the first 20 sec of HDT (from 66.8 +/- 9.9 min-1 to 60 +/- 11 min-1; p < 0.05). Transcutaneous pCO2 was within physiological ranges during the whole procedure (mean pCO2 minimum 39.5 +/- 2.9 mmHg, mean pCO2 maximum 42.2 +/- 3.3 mmHg). Mean CBFV did not change significantly during tilt (from 70.1 +/- 19.1 cm sec-1 to 66.6 +/- 14.1 cm sec-1; p > 0.05). PI, however, increased significantly with a more pronounced increase during the first 20 sec than the last 40 sec of tilt (PIsupine 0.92 +/- 0.11; PItilt(0-20 sec) 1.15 +/- 0.18; PItilt(21-60 sec) 1.03 +/- 0.16; p = 0.001; p = 0.017). The HDT results were found to be reproducible in the five volunteers. During 80 degrees-HDT mean BP and pCO2 did not change significantly. This observation combined with the significant decrease in heart rate during the first 20 sec of HDT, suggests that there is no sympathetic activation. The significant PI increase during HDT indicates a vasoconstriction of the cerebral resistance vessels. We assume that this vasoconstriction is due to the myogenic mechanism of cerebrovascular autoregulation triggered by a rapid, passive intracranial blood volume influx during HDT

BACKGROUND AND PURPOSE: Monitoring of the basilar artery (BA) is difficult and has been sparsely performed. The aim of this study was to present physiological data of functional transcranial Doppler sonography (TCD) of the BA during caloric vestibular stimulation in healthy volunteers. METHODS: TCD of the BA was performed in 26 healthy volunteers (14 women, 12 men, age 25.1+/-3 years) during caloric vestibular stimulation. Vertigo was documented using electronystagmography (ENG) and a subjective vertigo scale ranging from 0 to 10 points. Simultaneously, capnogpraphy was performed. RESULTS: All subjects experienced vertigo, nausea and oszillopsia during vestibular irrigation. The average subjective vertigo was for a period of 106 s (+/-65.4); the average subjective estimated degree of vertigo was 6.7 points (+/-1.5). In all subjects, ENG demonstrated horizontal nystagm to the left non-irrigated side. In 14 subjects the subjective vertigo was rated by the individuals as extreme (point score > or =7) and in 12 subjects as low (point score <7). Mean flow velocity (MFV) in the BA increased significantly during vestibular irrigation, being more prominent in the initial irrigation and vertigo phase (5.8+/-5.9%, P<0.05) than in the second vertigo phase (2.2+/-8.8%, P<0.05). The calculated pulsatility index (PI), which indicates the condition of the small resistance vessels, decreased significantly (-4.9+/-8.1%; 4.3+/-8.9%, P<0.05) during both phases of vestibular activation. End tidal pCO2 did not change significantly (constant 5.4+/-0.4 Vol%), but respiration frequency was significantly increased during vestibular stimulation (12.3+/-3.8 min(-1) to 16.4+/-5.3 min(-1) and 16.3+/-4.8 min(-1), P<0.05) probably as a vegetative sign of vertigo. The observed MFV- and PI-changes were more prominent, although not quite significant, in the subgroup of subjects who experienced extreme subjective vertigo than in the subgroup who experienced low subjective vertigo. CONCLUSION: These observations indicate that MFV increase in the posterior circulation is due to activation of the vestibulocerebellum. In addition, it is possible that the previously elaborated MFV increase in the MCA might contribute to MFV increase in the BA via the posterior communicating artery. The difference in the 2 subgroups (extreme vertigo vs. low vertigo) may reflect the great variety of anatomical and physiological conditions of the peripheral vestibular organ, the brainstem anatomy and the corresponding blood supply. For clinical purposes this TCD-test may contribute to the investigation of the vasomotor reserve of the posterior circulation, e.g. in patients with vertebrobasilar ischemia, bilateral vestibular loss or local neurodegenerative disease

In familial dysautonomia (FD), i.e., Riley-Day syndrome, parasympathetic dysfunction has not been sufficiently evaluated. The cold face test is a noninvasive method of activating trigeminal brain stem cardiovagal and sympathetic pathways and can be performed in patients with limited cooperation. We performed cold face tests in 11 FD patients and 15 controls. For 60 s, cold compresses (0-1 degrees C) were applied to the cheeks and forehead while we monitored heart rate, respiration, beat-to-beat radial artery blood pressure, and laser-Doppler skin blood flow at the first toe pulp. From these measurements heart rate variability parameters were calculated: root mean square of successive differences (RMSSD), coefficient of variation (CV), low- and high-frequency (LF and HF, respectively) power spectra of the electrocardiogram, and the LF transfer function gain between blood pressure and heart rate. All patients perceived cold stimulation and acknowledged discomfort. In controls, heart rate and skin blood flow decreased significantly during cold face test; in patients, both parameters decreased only briefly and not significantly. In controls, blood pressure, RMSSD, CV, and heart rate HF-power spectra increased but remained unchanged in patients. Respiration, as well as heart rate LF power spectra, did not change in either group. In controls, LF transfer function gain between blood pressure and heart rate indicated that bradycardia was not secondary to blood pressure increase. We conclude that the cold face test demonstrated that patients with FD have a reduced cardiac parasympathetic response, which implies efferent parasympathetic dysfunction

We investigated cardiac sympathetic innervation by metaiodobenzylguanidine (MIBG) imaging in a patient with tonic pupils, loss of tendon reflexes, and segmental anhidrosis (Ross syndrome). Despite normal cardiovascular reflex tests, we observed a reduced global myocardial MIBG uptake as well as a regional uptake defect over the posterolateral cardiac territory indicating left ventricular peripheral sympathetic denervation. MIBG imaging seems to be a useful noninvasive diagnostic method for detection of early--possibly subclinical--cardiac autonomic impairment in Ross syndrome and provides further evidence of injury to postganglionic autonomic neurons as the underlying pathological mechanism of the disease

OBJECTIVE: To evaluate whether sympathetic skin response (SSR) differs in patients with hereditary sensory autonomic neuropathy (HSAN) types III and IV. BACKGROUND: HSAN types III and IV are rare autosomal recessive disorders that cause many similar autonomic, sensory, and motor dysfunctions, but different sweating characteristics. HSAN III patients have preserved and at times, excessive sweating, whereas anhidrosis is characteristic of HSAN IV. SSR reflects the integrity of sympathetic sudomotor fibers and the activation of sweat glands through the change in skin resistance in response to an arousal stimulus. Therefore, SSR is a test method that might facilitate differential diagnosis of HSAN III and IV. METHODS: In 17 HSAN III patients (eight women, nine men; mean age, 20.65+/-5.45 years) and seven HSAN IV patients (five girls, two boys; mean age, 10.0+/-5.45 years) SSR was recorded from the palms and soles after repeated electrical, acoustic, and inspiratory gasp stimulations. In addition, all subjects underwent a neurologic examination; studies of median, peroneal motor, and sural nerve conduction velocities; and determination of vibratory and thermal perception thresholds. RESULTS: Although clinical differences were appreciated between the two types of HSANs, both HSANs had evidence of small-fiber involvement. Both HSANs had abnormal temperature and pain perception. In contrast, SSR was preserved in all HSAN III and absent in all HSAN IV patients. CONCLUSION: SSR provides another parameter to improve differentiation of HSAN III from HSAN IV, and also gives us additional information regarding sympathetic sudomotor fiber function in these developmental diseases