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A G7P5A1 woman in her 40s presented to the emergency department at 37 weeks 3 days’ estimated gestational age (EGA) with headache, lip tingling and several days of difficulty speaking. Physical examination demonstrated bilateral facial weakness in a peripheral distribution, as well as decreased corneal reflexes and cervical lymphadenopathy. Routine fourth generation HIV screening had previously been negative at 14 and 28 weeks’ EGA. Brain MRI was unremarkable, and lumbar puncture disclosed a low-grade, mononuclear cerebrospinal fluid pleocytosis; the patient was treated supportively. She returned for induction of labour at 39 weeks, at which time HIV infection was unexpectedly diagnosed. While unilateral idiopathic peripheral facial paralysis is associated with the third trimester of pregnancy and the early postpartum period, bilateral facial paralysis is rare and should prompt work-up for an underlying systemic cause, such as HIV infection.

Background The aetiology of blepharospasm remains unclear. There is evidence that the afferent pathway is important, but this area remains under-researched. Aim To explore the hypothesis that the afferent arm of the blink reflex is abnormal in blepharospasm by assessing a range of measures of corneal sensory function. Methods In this prospective case–control study, 21 patients with blepharospasm and 21 age-matched and gender-matched controls completed the Ocular Surface Disease Index questionnaire and underwent the following assessments: tear osmolarity, Shirmer test, tear-film break up time, corneal and conjunctival vital staining, meibomian gland dysfunction, corneal aesthesiometry and confocal microscopy. Results Corneal sensitivity was significantly lower in patients with blepharospasm than in controls (right eyes p=0.009; left eyes p=0.009, paired t test). The median number of main nerve trunks was lower for patients with blepharospasm than for controls, and this was statistically significant at the 5% level (p=0.04, paired t test). Mean nerve density, median number of nerve branches and median total number of nerves were lower for blepharospasm cases than controls, but this did not reach statistical significance. Tortuosity was greater for blepharospasm cases than controls, but this was not statistically significant. Conclusions Blepharospasm is associated with reduced corneal aesthesiometry and a tendency towards a reduced number of nerves in the sub-basal plexus, implying an impairment in corticosensory processing, possibly a defect of the sensorimotor gating mechanism resulting in a loss of inhibition of the blink reflex.

A 44-year-old, right-handed woman presented with a 2 year history of intermittent burning and numbness over the left side of her face which had become continuous for the past 9 months. Over the past 7 months she had experienced spasms characterised by a sensation that the left side of her mouth was being pulled tight, associated with spontaneous flexed posturing of the left elbow and wrist with clawing of the hand. The spasms lasted for approximately 15 s and were extremely painful. They occurred in paroxysms lasting up to 2 h, several times a week. One month prior to presentation, she developed double vision on looking to the left with vertical separation of the images, and vertigo. She also reported fatigue, dry mouth and dry eyes over the previous 2 years. There was no previous medical history and she was taking no medications. Family history was unremarkable. Examination showed a markedly dry mouth. There was no skin rash or joint inflammation. On left lateral gaze the left eye deviated upwards in comparison with the right, a left hypertropia. Eye movements were otherwise normal. There was subjective reduction in sensation over the left side of the face in all trigeminal nerve divisions, consistent with a sensory trigeminal neuropathy, with preservation of the corneal reflex. Neurological examination was otherwise unremarkable. Routine biochemistry and haematology were normal. P and C antineutrophil cytoplasmic antibodies, rheumatoid factor, tissue autoantibodies, extractable nuclear antigen antibodies, anti-scl-70, anticentromere, antiphospholipid, anti-Jo1, anti-Ro, anti-La, anti-RNP and anti-Sm antibodies were all consistently negative. Antinuclear antibodies were slightly raised at a titre of 1 in 40 but double stranded DNA antibodies were negative. MRI of brain and cervical spine with contrast was normal. Lumbar puncture showed normal opening pressure, protein, glucose and cell count, and was negative for oligoclonal bands. Chest x …

A 48-year-old woman presented with 8 months of right-sided burning facial pain and 4 weeks of unsteadiness. She had reduced right facial sensation and corneal reflex. She had no pyramidal or cerebellar signs. Examination of the other cranial nerves was unremarkable. She had reduced sensation in all modalities along the left side of her body. MRI showed a right-sided enhancing cerebellopontine angle lesion indenting the mid-pons contiguous with a thickened trigeminal nerve extending towards Meckel’s cave (figure …

To make electrophysiological observations on a large kindred with hereditary motor and sensory neuropathy-Lom (HMSN-L) containing 27 affected individuals.Onset was in early childhood with gait difficulty related to progressive lower limb weakness. Upper limb weakness developed later. Bulbar involvement was present in one third of the patients, and deafness appeared during the second or third decades. ELECTROPHYSIOLOGICAL FINDINGS: Electromyographic evidence of denervation was progressive, more severe distally, and greater in the legs, being total in distal lower limb muscles in most patients. Sensory action potentials were absent and motor nerve conduction was severely slowed. This included proximal upper limb (musculocutaneous and axillary), hypoglossal, and facial nerves. The severity of slowing increased during childhood. M waves, often multiple, were recorded in all affected individuals. The blink reflex showed an unusual three component response. The latencies of all three components were prolonged.HMSN-L is shown to be a demyelinating neuropathy involving severe and early axonal loss. The progressive slowing of nerve conduction during childhood differs from the static reduction seen in type I HMSN.

The palmomental reflex is considered to be one of the frontal release signs, also known as primitive reflexes.1 These reflexes include utilisation behaviour, grasping, rooting, sucking and snouting, but not pouting—any reflex involving a strike is a myotactic stretch reflex and indicates an upper motor neurone lesion.2 Present in some mammals where they may confer some survival benefits, these reflexes are thought to be present early in human development, to be supressed during cortical maturation, but to re-emerge in the presence of neurological disease affecting the frontal lobes. Typically elicited by gently scratching an orange stick from the proximal to distal aspect of the thenar eminence, a positive palmomental reflex is when there is a single synchronous contraction of the ipsilateral mentalis muscle, that is, a twitch at the chin.3 At face value, the palmomental reflex is perhaps the perfect stereotype of the neurologist's art: visually arresting …

OBJECTIVE—To investigate whether the human cerebellum takes part in fear conditioned potentiation of the acoustic blink reflex. METHODS—A group of 10 cerebellar patients (eight patients with lesions involving the medial cerebellum, two patients with circumscribed lesions of the cerebellar hemispheres) was compared with a group of 16 age and sex matched healthy control subjects. The fear conditioned potentiation paradigm consisted of three phases. During the first, habituation phase subjects received 20 successive acoustic blink stimuli. In the subsequent fear conditioning phase, subjects passed through 20 paired presentations of the unconditioned fear stimulus (US; an electric shock) and the conditioned stimulus (CS; a light). Thereafter, subjects underwent the potentiation phase, which consisted of a pseudorandom order of 12 trials of the acoustic blink stimulus alone, 12 acoustic blink stimuli paired with the conditioned stimulus, and six conditioned stimuli paired with the unconditioned stimulus. The EMG of the acoustic blink reflex was recorded at the orbicularis oculi muscles. The potentiation effect was determined as the difference in normalised peak amplitude of the blink reflex evoked by pairs of CS and acoustic blink stimuli and evoked by the acoustic stimulus alone. RESULTS—In the habituation phase, short term habituation of the acoustic blink reflex was preserved in all cerebellar patients. However, in the potentiation phase, the potentiation effect of the blink reflex was significantly reduced in patients with medial cerebellar lesions compared with the controls (mean (SD) potentiation effect (%), patients: −6.4 (15.3), controls: 21.6 (35.6)), but was within normal limits in the two patients with lateral lesions. CONCLUSIONS—The present findings suggest that the human medial cerebellum is involved in associative learning of non-specific aversive reactions—that is, the fear conditioned potentiation of the acoustic blink reflex.

OBJECTIVES—Pathways of late blink reflexes are detected by high resolution MRI. Electronically matched stroke lesions superimposed to an anatomical atlas show the suspected course. METHODS—Fifteen patients with infarction of the lower brainstem, MRI lesions and electrically elicited blink reflexes were examined. The involved structures in patients with R2 and R2c blink reflex changes were identified by biplane high resolution MRI with individual slices matched to an anatomical atlas at 10 different levels using digital postprocessing methods. RESULTS—The blink reflexes were normal in five of 15 patients (33%) and showed loss or delay of R2 and R2c to stimulation ipsilaterally to lesion (R2-i and R2c-i) in eight (53%). Loss or delay of R2-i/R2c-i was seen in lesions covering the entire trigeminal spinal tract and nucleus (TSTN) at at least one level. These infarctions were located more dorsally within the medulla. Patients with normal blink reflexes showed lesions sparing or involving the TSTN only partially. They more often had incomplete Wallenberg's syndromes and MRI lesions were located more ventrally. CONCLUSIONS—Using digital postprocessing MRI methods it was possible to identify central pathways of late blink reflex in patients with Wallenberg's syndrome. This method is suggested as a new approach to identify incompletely understood functional structures of the brainstem.

To evaluate the possible blink reflex responses in facial muscles reinnervated by the accessory nerve. Method: Eleven patients with a complete facial palsy were submitted to a surgical repair by an accessory facial nerve anastomosis (AFA). In this pathological group, blink reflex was studied by means of percutaneous electrical stimulation of the supraorbital nerve and recording from the orbicularis oculi muscle. A control group comprised seven normal people and seven patients with a complete Bell's facial palsy; in this group, responses on the sternocleidomastoideus (SCM) muscles were studied after supraorbital nerve stimulation. Results: All the patients with AFA showed a consistent degree of facial reinnervation. Ten out of the 11 patients with AFA showed reflex responses; in six, responses were configured by a double component pattern, resembling the R1 and R2 components of the blink reflex; three patients had an R1-like response and one patient showed a unique R2 component. Mean values of latencies were 15.2 (SD 4.6) ms for the R1 and 85.3 (SD 9.6) ms for the R2. In the control group, eight out of 14 people had evidence of reflex responses in the SCM muscles; these were almost exclusively configured by a bilateral late component (mean latency 63.5 (SD 15.9) ms) and only one of the subjects showed an early response at 11 ms. Conclusion: The trigemino-accessory reflex response in the pathological group was more complex and of a significantly higher incidence than in the control group. These differences could be tentatively explained by a mechanism of synaptic plasticity induced by the impairment of the efferent portion of the reflex. This could unmask the central linking between the trigeminal and the accessory limbs of the reflex. The findings described could be a demonstration of neurobionomic function in the repairing process of the nervous system. Sin financiación 2.735 JCR (1999) Q1, 25/132 Clinical Neurology, 16/80 Psychiatry, 10/131 Surgery UEM

Objective: In patients with hemifacial spasm (HFS), abnormal muscle responses (AMR) are frequently present. The objective of this study was to investigate whether the afferent input of AMR is mediated by antidromic facial nerve stimulation or orthodromic trigeminal nerve stimulation. Methods: AMR in the orbicularis oris muscle were recorded in 28 patients with HFS. When AMR were present, they were recorded after subthreshold stimulation of the facial nerve and weak stimulation delivered to the skin. Results: AMR were recordable in 24 (86%) of the patients, and usually consisted of the early constant component (mean onset latency, 10.0 ms) and late variable component (35.3 ms), similar to R1 and R2 of the blink reflex. The early or late components of AMR, or both, were frequently elicited after subthreshold stimulation of the facial nerve (43%) and skin stimulation (88%). Conclusions: AMR are likely to be mediated by trigeminal afferent inputs, rather than antidromic activation of the facial nerve, and are a type of trigeminal reflex.

During a 10 year period 24 patients with definite multiple sclerosis with isolated cranial nerve palsies were studied (third and fourth nerve: one patient each, sixth nerve: 12 patients, seventh nerve: three patients, eighth nerve: seven patients), in whom cranial nerve palsies were the presenting sign in 14 and the only clinical sign of an exacerbation in 10 patients. MRI was carried out in 20 patients and substantiated corresponding brainstem lesions in seven patients (third nerve: one patient, sixth nerve: four patients, eighth nerve: two patients). Additional abnormal findings of electro-oculography, or masseter reflex, or blink reflex, or combinations of these were found in 20 patients and interpreted in favour of a brainstem lesion at the level of the respective cranial nerve. In 11 of 14 patients with isolated cranial nerve palsies as the presenting sign of multiple sclerosis, dissemination in space was documented by MRI, and in the remaining three by evoked potentials. In patients with multiple sclerosis with isolated cranial nerve palsies, MRI is the most sensitive method of documenting dissemination in space and electrophysiological testing the most sensitive at disclosing brainstem lesions.

An experimental study and mathematical analysis of the corneal reflex test was undertaken in spectacle wearers. In the experimental study, photographs were taken of the corneal reflex through spectacles and the conversion ratios determined as measured in degrees/mm. In the mathematical analysis, the magnification effect of the lens was elucidated by three methods: geometrical analysis; real measurement of magnification factor; and ray tracing analysis. The real measurement of the conversion ratios was in good agreement with the conversion ratios determined by the three mathematical analyses. These results clearly showed that the corneal reflex test can be clinically useful even in wearers of spectacles.

Certain functions of the nervous system were examined in 31 printing workers (mean age 44) exposed to trichloroethene (mean duration 16 years) and 28 controls (mean age 45). In the sural nerve the conduction velocity (SNCV), response amplitude, and refractory period (SRP) were measured. The latencies of the masseter and the blink reflex were determined to test the trigeminal nerve. In the peroneal nerve the conduction velocity of fast and slow nerve fibres, the response amplitude, and the refractory period were determined. As a measure of autonomic nerve function the response of the heart rate was determined to isometric muscle contraction and deep breathing. Individual cumulative exposure was calculated on the basis of exposure levels in the past. The mean cumulative exposure of the exposed workers was 704 ppm x years. For the assessment of the exposure effect relation a multiple linear regression model was used. A slight reduction (-1.1 m/s) in the SNCV was found and a prolongation (0.4 ms) of the SRP (mean of the controls 1.95 ms). The latency of the masseter reflex (mean 10.4 ms) had increased (0.4 ms). With respect to the blink reflex no prolongation was found. No impairment was found in the functions of motor and autonomic nerves. This study shows that the refractory period may be a sensitive indicator of preclinical toxic neuropathies. Long term exposure to trichloroethene at threshold limit values (about 35 ppm) may slightly affect the trigeminal and sural nerves.

The electrically elicited blink reflex allows quantitative analysis of the corneal reflex which traverses the trigeminal and facial nerves and the brainstem. Two patients presenting with symptomatic unilateral trigeminal lesions are described, in whom the blink reflexes showed conduction block and slowing at predictable sites in the central pathways, and magnetic resonance imaging confirmed precisely the clinical and electrophysiological localisation.

A 57-year-old man presented with numbness, paraesthesia and lancinating pain on the left side of the face, which had developed suddenly 10 days previously. He had hypertension and no history of headache. His facial pain was characterised by a brief electric shock-like pain, which was evoked by light stimuli, and also occurred spontaneously. A neurological examination showed a mild decrease in sensation on the left side of the face, mainly with V2 and V3 distribution, and on the left oral cavity, including the tongue and buccal mucosa. Other neurological examinations were normal, including the corneal reflex and the motor component of the trigeminal nerve. MRI scan of the brain revealed the presence of a subacute ischaemic lesion in the left dorsolateral pons with the ipsilateral cisternal …

The body core temperatures of 31 patients suffering from severe cerebral lesions were measured. Evidence for the existence or nonexistence of circadian rhythms in these patients was found to be associated with diagnosis (acute versus chronic lesions), with the level of consciousness, and with neurological findings (such as best motor response and pupillary reaction), but not with heart rate, corneal reflex, initial Glasgow coma score (GCS), or outcome. This evidence came to light only after multiphasic mathematical transformations of the raw data.

Introduction Dystonia has historically been considered a disorder of the basal ganglia, however recent clinical and experimental observations promote the hypothesis that the dystonic neuroanatomical network is wider. In particular there is evidence that the cerebellum is a key structure within this network. 1 Eye blink conditioning is a well characterised experimental paradigm that is highly conserved across species and is dependent upon the cerebellum. Previously it has been shown that levels of eye blink conditioning are reduced in cervical and focal hand dystonia, which suggests impaired cerebellar function in these subsets of dystonia. 2 Method In this study we examined eye blink conditioning in 11 patients with genetically confirmed DYT–1 dystonia and five patients with DYT–6 dystonia. 15 healthy age matched controls were also studied. Eye blink conditioning consisted of the pairing of a conditioning stimulus (CS) (salient 2kHz, 400 ms auditory tone via binaural headphones) with a strong unconditioned electrical stimulus (US) (200 µs pulse width, 5×sensory threshold, supraorbital nerve) 400 ms after the conditioning stimulus in order to elicit a blink reflex. After repeated pairings, conditioned responses (consisting of an eye blink starting before the US) are usually seen in healthy subjects. Conditioning consisted of six learning blocks of 11 trials: trials 1–9 were always CS–US pairs, trial 10 was US only and trial 11 was CS only. The main outcome variable was the number of conditioning responses in the final block. Results In both patient groups eye blink conditioning was observed, but at the group level there was a trend for patients with DYT–1 dystonia to condition less well (Mann–Whitney test, p=.097) compared to patients with DYT–6 dystonia, who conditioned at a comparable amount to aged matched controls. Conclusions There is now compelling evidence from studies in animal models of dystonia that the cerebellum has a critical role in the pathophysiology of some forms of dystonia. However evidence for cerebellar involvement in humans with the primary form of the disease is less well established. Eye blink conditioning is a unique electrophysiological paradigm in its ability to test associative learning within the cerebellar circuitry. Although the current data do not reveal statistically significant differences between patients with DYT1 and the small group of patients with DYT6 dystonia currently studied, there is an interesting trend towards less conditioning in DYT1 compared with DYT6 mutation carriers, and recruitment of further DYT6 positive patients is ongoing. If confirmed, this trend fits with previous functional imaging and behavioural studies suggesting differences in cerebellar activation patterns during movement in DYT1 and DYT6 dystonia. There may well be important differences in pathophysiology between patients currently grouped within primary dystonia.

Down syndrome (DS) is one the most common genetic disorders. Little is known about the impact of visual disorders in DS on daily life. Our aim was to study the relation between the incidence of ocular manifestations and adaptive behaviour. Methods We performed a detailed medical history, including ocular disorders. We tested Hirschberg’s corneal reflex method, observed eye movements during fixation of a slowly moving object, cover test, and assessed the Vineland Adaptive BehaviourScales, as well as the Coloured Progressive Matrices. 52 DS individuals with an age range of 19 to 52 years. Results. We observed a high incidence of ocular anomalies (refractive errors in 59.2%, strabism in 51%, motility disorders in 63.3% and congenital bilateral cataract in 16.2%), not differing with age. The occurence of visual disorders did neither lead to total lower adaptive level nor show an influence on cognition. Daily living skills were significantly lower in individuals with not corrected disorders, but these individuals showed a significant high co-morbidity of autism with childhood onset. We observed a majority of individuals with an adaptive functioning above the average. Hyperopia and the presence of refractive errors were significantly more frequent in individuals with an adaptive level above the average. Conclusions. Visual disorders lead to a poorer performance in adaptive behaviour in individuals with DS and also autism. This suggests that early intervention on refractive errors and visuo-motor skills helps in the acquisition of daily living activities, which remain stable over the life-span. Therapeutic options for cataract need to be addressed early.

Brainstem reflexes were examined in 23 children treated with thiopentone infusion and correlated with serum thiopentone concentrations. The results suggest that if all brainstem reflexes are lost with a serum thiopentone concentration less than 40 mg/l, it is unlikely to be due to the thiopentone alone. Other causes including brain death need to be considered.

Editor,—Early surgical intervention has been reported to achieve closure of laser induced macular holes.1 2 We report a case of spontaneous closure of a laser induced macular hole indicating that surgery should not be undertaken before a reasonable period of observation. ### CASE REPORT A 24 year old physics postgraduate student accidentally sustained an injury to his right eye while aligning an 806 nm titanium-sapphire laser. The laser parameters were pulse energy 2 mJ, pulse duration 100 femtoseconds, and repetition rate 10 Hz. The duration of exposure was limited by his blink reflex. He noted immediate impairment of central vision in this eye. When examined by an ophthalmologist 2 days later, visual acuity was 6/18 in the right eye. Amsler testing demonstrated an absolute paracentral scotoma which was 1.5° in diameter and abutted fixation. A full thickness macular hole was present with loss of both neurosensory retina and retinal pigment epithelium (RPE). The hole was …

The exact location of the pontine gustatory pathway has not yet been clarified, probably because there are so few studies of taste in patients with well localised brainstem lesions.1-3 Here we report on a patient with isolated hemiageusia and trigeminal sensory neuropathy from a single small pontine lesion. A 46 year old woman experienced a burning sensation on the left side of the tongue. The next day she discovered a loss of taste on the entire left half of her tongue and numbness on the left side of her face. Neurological examination was normal except for hypaesthesia to pain, touch, and temperature sensation in all three divisions of the left trigeminal nerve, with decreased left corneal reflex and no weakness of masseters. Taste sensation was tested using separate solutions of 1.2 …

A crossed short latency component (R1) of the human blink reflex could be elicited in orbicularis oculi muscles to stimulation of the contralateral supraorbital nerve, when infraliminal conditioning stimuli were applied to various cutaneous afferents of the body (facial, upper and lower limbs). The crossed R1 responses appeared when the time interval between the conditioning and the test stimuli was of 30 to 40 ms, 50 to 65 ms and 95 to 110 ms for facial, upper and lower limbs afferents respectively. For the same time intervals, these conditioning volleys also exerted a facilitatory effect on the ipsilateral R1 responses. Furthermore, crossed R1 responses were also obtained during supraspinal facilitation induced by a voluntary contraction of the eyelids. These data show that crossed oligosynaptic trigemino-facial reflex connections exist in normal subjects, which become functional when adequate conditioning stimuli are available.

In a case of cephalic tetanus with left facial spasms and trismus, the repetitive stimulation of the left facial nerve at 3, 10 and 20 Hz showed no facilitation or decrement. The amplitudes of the blink reflex were 50% lower on the affected side. The silent period of the masseter muscles was shortened. Concentric needle examination of the masseters and left facial EMG of the left frontalis muscle showed increased jitter and blocking in a significant proportion of the recorded potentials. Both jitter and blocking improved on higher innervation rates. All electrophysiological findings were normal on the second examination when the patient was asymptomatic. The single fibre EMG findings point to a presynaptic defect in the neuromuscular transmission in human tetanus.

The reflex responses evoked by direct electrical stimulation of the intracranial portion of the trigeminal nerve have been studied in 16 subjects undergoing percutaneous retrogasserian thermocoagulation for the treatment of trigeminal neuralgia affecting the second or third division. In the obicularis oculi muscle, early and late responses similar to the R1 and R2 components of the blink reflex were recorded. The former could be evoked only by stimulation of the second division and its latency was consistent with intermediately fast afferents. A late reflex (50-70 ms) was occasionally recorded from the anterior belly of the digastric muscle. The response was sometimes followed by a later activity and showed the features of a polysynaptic reflex. No response was obtained in the jaw elevators when fully relaxed. With the subject voluntarily clenching his teeth, both an early "H-like" response and two silent periods in the background EMG were obtained. The second silent period was similar in the muscles ipsi- and contralateral to intracranial stimulation, while the first silent period was longer in the ipsilateral muscles. Possible mechanisms contributing to the inhibition following stimulation of the mixed portion of the nerve are discussed.

Suppression of the vestibulo-ocular reflex was assessed in normal subjects and patients with neurological disorders to determine the relative effects on suppression of a single fixation target and an optokinetic field. Subjects were rotated sinusoidally in yaw at varying frequencies of up to 0.5 Hz whilst seated in a Barany chair. A comparison was made between eye movements in darkness, those produced during fixation on a central target mounted to the chair, and eye movements during fixation on the target plus an "earth-fixed" or "chair-fixed" visual background. Presentation of a background produced only minimal effects on the suppression of the vestibulo-ocular reflex in normal subjects. In patients with impairment of fixation suppression, suppression of the vestibulo-ocular reflex was not improved after presentation of either form of optokinetic field. The results demonstrate that central fixation is the predominant requirement for suppression of the vestibulo-ocular reflex. This correlates closely with the ability to pursue. Although the optokinetic reflex generates following eye movements similar to pursuit, it cannot be used to mediate suppression of the vestibulo-ocular reflex in the absence of an intact pursuit system. The findings strengthen the view that the optokinetic reflex evolved to act in synergy with the vestibulo-ocular reflex in generating compensatory eye movements.

Latency variation of consecutive responses of single orbicularis oculi motoneurones in the first component of the electrically elicited blink reflex was 2.6 times larger than that of the H reflex of the soleus muscle fibres. Some motoneurones showed bimodal latency distribution or double responses or both at an interval of about 4-5 ms. Typical first component responses were sometimes obtained by contralateral stimulation. Central conduction time in the brainstem, estimated for 15 motoneurones, was between 2.4 and 6.6 ms. It is concluded that the first component of the blink reflex is conducted through an oligosynaptic arc including one or more interneurones.

In a patient with reflex myoclonus limited to the right side of the body, stimulation of the right median nerve in the index finger or wrist elicited a very large somatosensory evoked response (SER) and a long loop C reflex which represents an electrically evoked myoclonic response. It is suggested that the pathway for the C reflex is through peripheral nerve, dorsal funiculus of spinal cord, contralateral VP nucleus of thalamus, sensorimotor cortex, corticospinal tract, and anterior horn cell. The large SER, C reflex, and myoclonic jerks are presumed to result from a release effect causing increased excitability at central synapses along this pathway. The patient presented has a large atrophic vascular lesion involving the left frontotemporoparietal region and involvement of pathways through the right superior cerebellar peduncle to account for the neural dysfunction.

The corneal and blink reflexes were evaluated in 20 normal subjects and in 30 patients with motor deficits secondary to unilateral hemispheral lesions of vascular origin. In the normal population there were no differences between subjects below and subjects above 50 years of age. In the patients the reflex evoked by electrical stimulation of the cornea of the clinically affected side was depressed in 24 out of 30 cases. The depression mainly affected the afferent branch of the circuit, which triggers both homolateral and contralateral orbicularis oculi discharge (afferent abnormality). In three cases the depression was exerted concomitantly on the efferent branch (afferent and efferent abnormality) and only in one case was it limited to the efferent branch (efferent abnormality). The late R2 component of the blink reflex was depressed in 15 out of 30 patients. The early R1 component was slightly facilitated on the affected side. The changes of the corneal reflex and of the R2 component of blink reflex were similar, but the blink reflex had a greater safety factor. The patients with an abnormal corneal reflex had more extensive damage than had the patients with normal corneal response, as shown by computer tomography, but the site of the lesion was comparable in the two groups. Conduction through the brain stem circuits mediating the orbicularis oculi response is normally under pyramidal facilitatory influences while facial motoneurons are subjected to pyramidal inhibition. After pyramidal damage the transmission of impulses in the brain stem was slowed down, ultimately to a degree that abolished the reflex. Removal of pyramidal inhibition on facial motoneurons is probably the basis of the slight facilitation of the R1 component of the blink reflex.

Electrophysiological analysis of the blink reflex makes it possible to quantitate the reflex changes observed in pathology. The authors therefore propose a `habituation index' to be determined by recording the electromyographic reflex response during stimulation at controlled frequencies. Several populations of subjects were tested. It was confirmed that marked differences in blink reflex habituation exist between normals and patients with Parkinson's disease. It was also found that when patients with Parkinsonism were treated with the classical anticholinergic drugs their habituation index remained virtually unchanged. However, treatment with either l-dopa or amantadine caused a rise in the index in almost all patients tested. On the basis of these findings it is suggested that these two new drugs have a highly similar mechanism of action.

The contralateral corneal reflex may be absent in patients with a deep lesion of the parietal lobe. Frontal and temporal lobe lesions apparently do not interfere with this reflex.

The different effects of regular and stochastic stimulation on the flexor reflex of patients with the spinal cord totally divided and of normal subjects and on the blink reflex of normal subjects were studied. When the cutaneous stimulus was above but less than twice threshold, with regular stimulation habituation occurred; with stochastic stimulation, habitutaion either did not occur or it was minimal. Stochastic stimulation was at random stimulus intervals or with random stimulus intensities. When stimulus intensity was around threshold, habituation occurred with both kinds of stimulation, the response to stimulation soon ceasing to occur. When stimulus intensity was greater than twice threshold, habituation did not occur with both kinds of stimulation. When regular stimulation was given after the response had ceased to occur, extinction of the response beyond zero occurred. When a dishabituating stimulus was repeatedly applied in a regular manner, habituation to the dishabituating stimulus occurred. With regular and stochastic stimulation given as conditioning and test series, it was seen that stochastic stimulation caused, in addition to the short-term excitatory effect, the same long-term cumulative depressing effect on excitability as did regular stimulation.

The changes of threshold and receptive field of the Babinski reflex, with time, were assessed in ten patients with acute cerebrovascular lesions. It was found that the threshold of the reflex decreased gradually and the size of the cutaneous afferent reflex field enlarged with the passage of time. These findings suggest that there is a gradual release or organisation of the reflex flexor synergy of which the Babinski sign is a modified part.

Thirty-nine patients with trigeminal neuralgia, not controlled by medical treatment, were treated by radio-frequency thermocoagulation of the Gasserian ganglion and its posterior rootlets. Thirty-six received satisfactory pain relief. In 30 patients touch sensation in the treated territory was preserved. The corneal reflex was affected in only six patients, two of whom subsequently developed keratitis. There were no other complications apart from a minor unpleasant sensation in eight patients. By selectively destroying pain fibres this technique offers the scope of preserving touch sensation in the treated area. Moreover, the zone of analgesia can be restricted to the affected region by sensory mapping through electrode stimulation before thermocoagulation. Its simplicity, low morbidity, associated short hospital stay, and the increased ability to preserve touch sensation, especially of the cornea, seem to make it preferable to other forms of surgical management for trigeminal neuralgia.