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The significance of a crossed extensor hallucis response on active flexion of the hip was analysed in various neurological disorders. It is concluded that this sign, not formerly described, is a pathological reflex or synkinesia. In the cooperative patient the crossed extensor response is a more sensitive indicator of a minor disturbance within the cortico-spinal motor pathways than the Babinski sign. With lesions above the foramen magnum a crossed extensor hallucis response is observed more frequently than the Babinski sign.
The electromyographic activity in several leg muscles during the elicitation of "the crossed up-going toe sign" (CUT) was studied in patients and compared with that obtained in connection with the Babinski sign and in normal subjects. The results indicate that the patterns of activation and the responsible pathways are different for the CUT and Babinski signs. The difference between the normal subjects and the CUT positive patient is a matter of quantitative difference of coactivation of distal leg muscles during the test procedure rather than a change of reflex patterns.
The Babinski reflex and the CUT reflex were examined in 150 neurological patients and 20 controls. A positive CUT reflex occurred more frequently than a positive Babinski reflex in the patient material as a whole, and in different diagnostic groups. However, there was a low grade of correspondence between a positive CUT reflex and a positive Babinski reflex. There were many positive CUT reflexes in the group of normal persons. In a number of cases the examination of the CUT reflex was impossible because of lack of strength or incooperability. The study indicates that the CUT reflex and the Babinski reflex are not comparable phenomena.
Two patients with reflex reticular myoclonus [RRM] were tested electrophysiologically and pharmacologically. In one of the cases the underlying disease was chronic Lyme borreliosis. In the other, the RRM attacks may have been associated with procarbazine therapy applied for Hodgkin's disease. No cortical lesion could be demonstrated either clinically or electrophysiologically [EEG, averaged EEg preceeding the jerks, SSEP]. An EMG analysis of the jerks revealed the shortest latency in the muscles innervated by the accessory nerve. The latencies became longer in a more rostral muscle [masseter], as well as in a more caudal one, the muscles innervated by the facial nerve were spared. it is presumed that the complete movement pattern of the myoclonus residues in the jerk generating structure. RRM in the described cases differs from the startle by sparing the facial nerve and from the Papio papio baboon non-epileptic myoclonus by the activating effect of physostigmine. A partial therapeutic effect was achieved with a serotonine precursor, but a GABAergic therapy proved to be the most effective.
T-wave responses of biceps and triceps brachii muscles were recorded electrophysiologically from 31 normal subjects and 15 patients with unilateral lesions of the cervical C6 or C7 roots. Pathological T-wave responses were found in 11 (73%) patients. Patients with radiological correlate showed electromyographic (EMG) pathology in 60% but a pathological T-wave response in 90%. All patients with radiological correlate also showed pathological electrophysiological tests (EMG or T-wave responses). Electrophysiological measurement of the T-wave response appears to be a potentially useful tool in the diagnosis of cervical radiculopathies.
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The present report describes a benign disorder of neonates or young infants presenting with generalized hypertonicity accompanied by brisk muscle stretch reflexes, intermittent clonus, and exaggerated startle response. This condition is termed hyperexplexia, and may be either familial or sporadic. Two affected families are reported: Two sisters and their mother are involved in the first family; in the second family, where the parents are asymptomatic first degree cousins, all three siblings suffer from hyperexplexia of various severity. Nose tapping in infants of affected families induced a uniform reaction of facial twitching accompanied by head extension, and a generalized flexor spasm, all of which may be a hallmark of hyperexplexia. Severely hypertonic infants were treated with small doses of benzodiazepines and improved markedly, all becoming asymptomatic by two years of age. Unnecessary investigation and treatment may be avoided by sufficient awareness of possible hyperexplexia.
Startle disease or hyperreflexia is an autosomal dominant neurological disorder, with a neonatal onset, characterized by muscular hypertonia and myoclonic jerks, exaggerated by the slightest stimulus. Low concentrations of free gamma-aminobutyric acid (GABA) have been found in the cerebrospinal fluid of two affected infants. The involvement of GABA or its receptors has been raised and the use of GABA-agonist drugs has been suggested. We report a newborn with startle disease who also had a low concentration of GABA in the cerebrospinal fluid. No clinical improvement was observed with progabide, a GABA agonist. Furthermore, a high dose (100 mg/kg) of gamma-hydroxybutyrate (GHB) did not improve muscular stiffness and failed to induce general anesthesia. GHB, currently used as an effective general anaesthetic, is a structural analogue of GABA. It is present naturally at low concentrations in the brain and is regarded as an inhibitory neurotransmitter. Two specific GHB receptors, distinct from the GABA receptors, have been identified in rat brain. Failure to induce general anesthesia with a high dose of GHB suggests that one of these receptors could be involved in startle disease.
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In two recent studies, we found autonomic nervous hyperreflexia in subjects with chronic inflammatory diseases, particularly, in those subjects with higher degrees of systemic inflammation. Since corticotropin-releasing factor (CRF) is induced by inflammatory stimuli and acts within the brain to change neuroendocrine and autonomic activity, we investigated CRF modulation of standard autonomic nervous reflexes. Fifteen healthy subjects were administered 100 microg CRF i.v., which led to a short-term increase of heart rate (p < 0.001) and a decrease in systolic and diastolic blood pressure (p < 0.050). These changes were accompanied by a reduction in heart rate variation at rest (p = 0.010) and during the respiratory sinus arrhythmia test (p = 0.019), and a reduction of pupillary latency time (p = 0.038). In further 21 normal subjects we studied the effect of prednisolone treatment on autonomic nervous function (100 mg/d during three days --> CRF reduction), which resulted in an increase of heart rate (p < 0.001), increase of heart rate variation during the respiratory sinus arrhythmia test (p < 0.001), increase in pupillary latency time (p = 0.012), a increase in maximal pupillary area (p = 0.002), and a decrease in diastolic blood pressure (p = 0.002). In conclusion, induction of a low central CRF content by prednisolone leads to a marked hyperreflexia in respiratory sinus arrhythmia and hyporeflexia in the latency time test. It is obvious that CRF can regulate autonomic reflexes. Possibly, central CRF status may also influence autonomic reflexes during chronic inflammation due to chronically changed central CRF concentration.
Recent evidence suggests that alterations in ionic conductances in spinal motoneurones, specifically the manifestation of persistent inward currents, may be partly responsible for the appearance of hyperexcitable reflexes following spinal cord injury (SCI). We hypothesized that such alterations would manifest as temporal facilitation of stretch reflexes in human SCI. Controlled, triangular wave, ankle joint rotations applied at variable velocities (30-120 deg s(-1)) and intervals between stretches (0.25-5.0 s) were performed on 14 SCI subjects with velocity-dependent, hyperexcitable plantarflexors. Repeated stretch elicited significant increases in plantarflexion torques and electromyographic (EMG) activity from the soleus (SOL) and medial gastrocnemius (MG). At higher velocities (> or = 90 deg s(-1)), reflex torques declined initially, but subsequently increased to levels exceeding the initial response, while mean EMG responses increased throughout the joint perturbations. At lower velocities (< or = 60 deg s(-1)), both joint torques and EMGs increased gradually. Throughout a range of angular velocities, reflex responses increased significantly only at intervals < or = 1 s between stretches and following at least four rotations. Ramp-and-hold perturbations used to elicit tonic stretch reflexes revealed significantly prolonged EMG responses following one or two triangular stretches, as compared to single ramp-and-hold excursions. Post hoc analyses revealed reduced reflex facilitation in subjects using baclofen to control spastic behaviours. Evidence of stretch reflex facilitation post-SCI may reflect changes in underlying neuronal properties and provide insight into the mechanisms underlying spastic reflexes.
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