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There has recently been a marked rise in the medicinal use of cannabis for epilepsy and multiple other conditions. While seizures have been reported in association with synthetic cannabinoids, the clinical features and prognosis have not been studied. Thirty patients with a history of seizures occurring within 24 h of synthetic cannabinoid use were identified from a first seizure clinic database in Perth, Western Australia between 2011 and 2016. Eight had a prior history of seizures, three related to synthetic cannabinoid use, with an additional three patients having risk factors for seizures. The presenting event was a tonic–clonic seizure in 27 patients (90%). “Kronic” was the synthetic cannabinoid used by 16 patients. Absorption was via smoking in all cases, with seizures occurring within 30 min of inhalation in 14 patients (46%). Electroencephalography (EEG) showed epileptiform abnormalities in 11%, and neuroimaging revealed epileptogenic lesions in 12%. Nine of 24 patients with follow-up had subsequent seizures, occurring in the setting of further synthetic cannabinoid use in two patients. This seizure recurrence rate is similar to seizures provoked by other acute systemic insults. In conclusion, smoking of some synthetic cannabinoids is associated with seizures, and this may relate to an intrinsic proconvulsant effect.

Anterior knee pain is a highly prevalent condition affecting largely young to middle aged adults. Symptoms can recur in more than two thirds of cases, often resulting in activity limitation and reduced participation in employment and recreational pursuits. Persistent anterior knee pain is difficult to treat and many individuals eventually consider a surgical intervention. Evidence for long term benefit of most conservative treatments or surgical approaches is currently lacking. Injection of Botulinum toxin type A to the distal region of vastus lateralis muscle causes a short term functional “denervation” which moderates the influence of vastus lateralis muscle on the knee extensor mechanism and increases the relative contribution of the vastus medialis muscle. Initial data suggest that, compared with other interventions for anterior knee pain, Botulinum toxin type A injection, in combination with an active exercise programme, can lead to sustained relief of symptoms, reduced health care utilisation and increased activity participation. The procedure is less invasive than surgical intervention, relatively easy to perform, and is time- and cost-effective. Further studies, including larger randomized placebo-controlled trials, are required to confirm the effectiveness of Botulinum toxin type A injection for anterior knee pain and to elaborate the possible mechanisms underpinning pain and symptom relief.

To examine long-term outcomes of Botulinum toxin type A (BoNT-A) injection to vastus lateralis (VL) for refractory anterior knee pain (AKP).Two cohorts (private clinic referrals and previous research participants) injected with BoNT-A for AKP by one neurologist were surveyed retrospectively. Primary outcomes were self-reported benefit, duration of symptom relief, and knee surgery post-injection. Secondary outcomes were changes in utilization of medication/physiotherapy treatment, AKP symptoms and activity limitation.Overall, average symptom duration was 76 months (SD 98). Responses were available from 46 of 53 private patients. Thirty-eight reported benefit from injection, which was ongoing in 29. Average benefit was 25 months (SD 21). Nine individuals reported symptom recurrence after an average of 14 months (SD 21). Ten had knee surgery post-injection; six of whom had not benefitted from BoNT-A injection. Nineteen of 23 previous research participants were contactable. Initially, all responded favorably to injection. Symptomatic benefit, with an average duration of 44 months (SD 20), persisted in 15. Two subjects proceeded to surgical intervention.A single BoNT-A treatment to VL led initially to improved function and relief of knee-related symptoms in 57 of 65 individuals. Improvements were sustained at follow-up, with an average benefit of 34 months (SD 25) post-injection, in 44 of 57 cases.

Objectives This randomised controlled crossover trial examined the efficacy of botulinum toxin type A (BoNT-A) injection, plus an exercise programme, to remediate chronic anterior knee pain (AKP) associated with quadriceps muscle imbalance. Methods 24 individuals with refractory AKP received either BoNT-A (500 U Dysport) or the same volume saline injection to the vastus lateralis (VL) muscle and performed home exercises focusing on re-training the vastus medialis (VM) muscle. All subjects were offered open-label injection at 12 weeks. Knee-related disability (anterior knee pain scale; AKPS) and activity-induced pain (10 cm visual analogue scale) at 12 weeks were the primary outcomes. Peak isometric extensor force was recorded and normalised VL:VM ratios were derived from simultaneous surface electromyography. Selfreported pain and disability measures were collected at six time points to a mean of 20±8 months. Results 14 subjects received BoNT-A and 10 placebo injection. Improvement at 12 weeks was significantly greater for BoNT-A compared with placebo-injected subjects for the AKPS (p

Intramuscular injection of botulinum toxin (BoNT) produces reversible blockade of neuromuscular transmission. In animal experimental models, recovery begins within four weeks and is usually complete by twelve weeks. We present evidence of prolonged denervation following BoNT injection of the vastus lateralis (VL) muscle to correct quadriceps muscle imbalance in patients with chronic anterior knee pain. Needle electromyography data were obtained from 10 subjects who had received a single BoNT treatment 5 to 19 months earlier as part of a clinical trial. Insertional and spontaneous activity, recruitment, and motor unit action potentials were examined. Clear differences between the injected and non-injected VL muscles, which correlated with the time since injection, were identified in all subjects. All 10 subjects studied with needle EMG showed evidence of persisting denervation in the BoNT-A injected VL muscle beyond the period of neuromotor recovery expected from animal experimental studies.

To examine the effect of intramuscular injection of botulinum toxin type A [Dysport] to reduce relative overactivity of the vastus lateralis [VL] muscle, in conjunction with re-training of vastus medialis [VM] muscle as an adjunct to rehabilitation for chronic anterior knee pain.Eight females with chronic (6 months) history of anterior knee pain, who had failed conservative management, were studied in this open label pilot study. Intramuscular Dysport injection [300 - 500 units] to the distal third of VL muscle was followed by a 12-week customized home exercise programme to improve recruitment of VM muscle and functional knee control. VL and VM muscle cross sectional area from a standardized spiral CT sequence, isometric quadriceps strength (dynamometry), timed stair task, self-reported pain and disability were assessed.Subjects reported reduced knee pain and brace dependency and increased participation in sporting and daily living activities. Isometric quadriceps muscle strength was maintained or improved despite significant atrophy, evident on CT, of the distal component of VL in the treated limb. Time taken to ascend and descend a flight of stairs improved in all subjects. Subjective and objective improvements were maintained at 24-week follow-up.These pilot data provide preliminary support for the role of Dysport as an adjunct to non-surgical management of individuals with chronic anterior knee pain. Larger double blind, randomized, placebo-injection controlled studies of this novel approach to improving patellofemoral mechanics are needed to establish the efficacy of this intervention.

Lingual or inferior alveolar nerve (IAN) injury after dental procedures may result from direct trauma or local anesthetic agent and presents with immediate onset of typically nonprogressive symptoms, including pain and sensory changes. We report a case of delayed-onset pain and progressive sensory symptoms after IAN block for amalgam restoration. A 54-year-old man presented with progressive right-sided facial pain 48 hours after IAN block for amalgam restoration, followed 1 week later by hypoesthesia and allodynia in IAN distribution. The presentation is more consistent with inflammatory neuropathy, as is well recognized in brachial plexopathy. Imaging was used to exclude local and central causes, following which the clinical diagnosis was made. Inflammatory neuropathies may be distinguished from iatrogenic causes on the basis of delayed symptom onset, early severe pain, and progressive sensory symptoms. Awareness of this condition is important, because early steroid therapy followed by medications for neuropathic pain may provide benefit.

Background: Stroke is a devastating complication of cardiopulmonary bypass (CPB) surgery which occurs in 1 to 5% of cases. Strategies to reduce its incidence require a knowledge of the underlying pathology and aetiology. Aims: To determine the incidence, pathology and aetiology of stroke complicating CPB. Methods: Prospective review of clinical, operative and cranial CT scan findings in all cases of stroke complicating CPB procedures in our institution over an 18 month period. Results:. Twenty-one (1.6%, 95% CI 0.9–2.3%) cases of stroke were identified from 1336 CPB procedures. Cranial CT scan, performed in all but one patient, was normal in three patients or consistent with ischaemic stroke in 17 patients. There were no cases of haemorrhagic infarction or intracerebral haemorrhage. It was difficult to differentiate embolic and borderzone infarcts in two cases. After considering the clinical, operative and CT scan features together, 12 (57%, 95% CI 36–78%) of the cases were felt to be embolic in origin and nine (43%, 95% CI 22–64%) due to hypoperfusion in a borderzone. Conclusions: This study demonstrates that stroke remains an important complication of CPB procedures with an incidence in our series of 1.6%. The pathologic type of stroke is predominantly ischaemic in nature due to either cerebral embolism or borderzone infarction. Strategies for stroke prevention in patients undergoing CPB should be targeted primarily at these two mechanisms.

There is a definite relationship between the vascular type of benign sexual headache and benign exertional headache. Forty five patients with benign vascular sexual headache were reviewed. Twenty seven (60%) experienced benign vascular sexual headache alone and eighteen (40%) had experienced both benign vascular sexual headache and benign exertional headache on at least one occasion. The mean age was 34.3 years with a male:female ratio of 5.4:1. Thirty patients with a history of benign vascular sexual headache were followed for an average of 74 months. A personal history of migraine was found in 47% of cases and a family history of migraine in 30%. Forty one per cent of patients with benign vascular sexual headache alone had recurrences after diagnosis, and stress and fatigue were considered major contributing factors to the initial and recurrent headache. Nine patients had experienced benign vascular sexual headache and benign exertional headache within 72 hours of each other on at least one occasion, often with a residual headache between the two. Four patients experienced their benign vascular sexual headache and benign exertional headache separated by months to years. The prognosis of benign vascular sexual headache and the clinical and possible pathophysiological relationships between benign vascular sexual headache and benign exertional headache are discussed. Knowledge of the interrelationships of these varieties of headache is valuable in the counselling of patients.

The patient concerned was a 36-year-old right-handed male who suffered 35% total body surface area burns (10% full thickness) post-self-immolation, affecting his face, anterior neck and torso, bilateral arms and left leg. He had no significant past medical history apart from depression and there was no history of alcohol dependence. He was admitted for a total of 42 days and spent 13 days in the intensive care unit, intubated and ventilated for 12 of these. On admission, he was significantly hypothermic and acidotic. Escharotomies of bilateral forearms and left thigh were performed within 21/ 2 h of admission (Fig. 1). Debridement and skin grafting was carried out on day 8 and day 26. His clinical course was complicated early by episodes of sepsis requiring inotropic support, coagulopathy, neutropaenia, acute respiratory distress syndrome and electrolyte disturbances. Once stable on the ward he made progressive recovery until discharge on day 42. One month after discharge, he re-presented with a history of acute pain and weakness in his right shoulder without obvious provocation. He described waking at 2 a.m. with a sharp pain in his shoulder but was able to move it normally. With simple analgesia he went back to sleep to wake 6 h later pain free but with weakness of his right shoulder. On examination, he had weakness of right shoulder abduction, and external rotation with power grade 0–1/5 (Fig. 2). He had

SUMMARY 1. Based largely upon in vitro studies, vitamin E has been reported to inhibit phospholipase A2 activity, to alter phospholipid metabolism and reduce platelet aggregation. 2. The effect of dietary supplementation with D-α-tocopherol (1500 iu/day for 14 days) was studied in nine males, 41–63 years old, comparing active treatment with a preceding placebo period. 3. Despite an increase from 2.6±0.8 (s.d.) × 10-5 mol/L to 6.0±1.8 10-5 mol/L in plasma vitamin E there were no significant changes in the aggregation of diluted whole blood or platelet rich plasma to adenosine diphosphate (ADP) or collagen, in plasma phospholipase A2 activity or plasma lyso-platelet-activating factor (lyso-PAF) (bioassay after in vitro acetylation to PAF). 4. High dose vitamin E dietary supplementation had no effect on these phospholipid and platelet parameters.

Intramuscular injection of Botulinum toxin to produce reduction of focal muscle overactivity, and localized muscle spasm, has been utilized therapeutically for almost two decades. Muscle overactivity in neurologically normal muscle, where an imbalance exists between a relatively overactive muscle and its less active synergist or antagonist, can inhibit control of the antagonist producing a functional muscle imbalance. This brief review provides an overview of the role of muscle imbalance in sports-related pain and dysfunction, and outlines the potential for intramuscular injection of Botulinum toxin to be used as an adjunct to specific muscle re-education and functional rehabilitation in this patient group. A comprehensive understanding of normal movement and the requirements of the sporting activity are essential to allow accurate diagnosis of abnormal motor patterns and to re-educate more appropriate movement strategies. Therapeutic management of co-impairments may include stretching of tight soft tissues, specific re-education aimed at isolation of the non-dominant weak muscles and improvement in their activation, 'unlearning' of faulty motor patterns, and eventual progression onto functional exercises to anticipate gradual return to sporting activity. Intramuscular injection of Botulinum toxin, in carefully selected cases, provides short term reduction of focal muscle overactivity, and may facilitate activation of relatively 'inhibited' muscles and assist the restoration of more appropriate motor patterns.

Five patients presented with symptoms related directly to pressure effects from their cavum septum pellucidum with persistent or intermittent obstructive hydrocephalus. The most characteristic presenting symptoms were intermittent postural headache and postural loss of consciousness. If cysts of the cavum septum pellucidum are symptomatic and stereotactic cyst puncture or fenestration are ineffective, ventriculoperitoneal shunting should be carried out before resorting to more radical excision of the cyst.

SUMMARY A 60-year-old man presented with sudden onset of left shoulder pain followed 2 weeks later by the development of left shoulder girdle weakness. A clinical and electrophysiological diagnosis of subacute idiopathic brachial neuritis was made. The MRI features of subacute muscular denervation in this patient are discussed and the relevant literature reviewed.

We read with interest the recent report by Padua et al 1 on a body building champion with an isolated mononeuropathy of a distal branch of the femoral nerve, having recently seen a similar patient, with a different cause. A 39 year old sports physiologist underwent a resting muscle biopsy using the Bergstrom technique, for research purposes. He had previously undergone eight of these biopsies on the other leg without adverse effect, and this biopsy was performed by an experienced operator. Under lignocaine anaesthesia the biopsy needle was inserted. As manual suction was applied followed immediately by closing the biopsy needle, the subject had an intense feeling of cramp (that had not been noticed with previous biopsies). The …

The acute onset of neck pain and arm weakness is most commonly due to cervical radiculopathy or inflammatory brachial plexopathy. Rarely, extracranial vertebral artery dissection may cause radiculopathy in the absence of brainstem ischemia. We describe a case of vertebral artery dissection presenting as cervical radiculopathy in a previously healthy 43-year-old woman who presented with proximal left arm weakness and neck pain aggravated by movement. Cervical magnetic resonance imaging (MRI) and angiography revealed dissection of the left vertebral artery with an intramural hematoma compressing the left C5 and C6 nerve roots. Antiplatelet treatment was commenced, and full power returned after 2 months. Recognition of vertebral artery dissection on cervical MRI as a possible cause of cervical radiculopathy is important to avoid interventions within the intervertebral foramen such as surgery or nerve root sleeve injection. Treatment with antithrombotic agents is important to prevent secondary ischemic events.

Cerebral amyloid angiopathy accounts for approximately 10% of spontaneous intracerebral hemorrhage, typically in the cortex and subcortical white matter. Its contribution to primary pontine hemorrhage is not known. The present study was designed to determine if amyloid angiopathy occurs in the pons and whether primary pontine hemorrhages are associated with amyloid infiltration of nearby vessels. Two groups of patients were identified. Group A included 30 patients with proven CAA in whom special blocks of the pons were taken, group B consisted of 10 primary pontine hemorrhages in whom transverse blocks were available. A congo red stain and an A4 immunohistochemical technique were used. Only 1 patient from group A and none from group B had amyloid angiopathy in the pons. It is concluded that pontine angiopathy is rare and an exceptional cause of primary pontine hemorrhage.

OBJECTIVE To report a case of cerebral neurocysticercosis, in which cranial magnetic resonance imaging (MRI) was performed at the time of probable death of the cysticercus. CLINICAL FEATURES A 15-year-old Indian boy with a focal seizure disorder presented with a low-grade fever and an increase in seizure frequency. Cranial MRI scanning demonstrated a small, cortically based nodule surrounded by a low-intensity ring and extensive oedema. INTERVENTION AND OUTCOME Carbamazepine therapy was continued (without steroids) and a further MRI scan after one month showed resolution of the oedema, and a subsequent cranial CT scan showed calcification of the cortically based nodule. Praziquantel therapy was administered. CONCLUSIONS Diagnosis of neurocysticercosis must often rely upon clinical and distinctive radiological findings. Death of the cysticercus may provoke an inflammatory reaction that may result in an increase in seizure frequency.

A case of dissection of the abdominal aorta in a 32-year-old Caucasian man associated with a histological diagnosis of granulomatous aortitis and a clinical diagnosis of idiopathic medial aortopathy is described. The relationship between giant cell "temporal" arteritis, Takayasu's disease and idiopathic medial aortopathy is discussed.

Breath-holding spells can be a source of considerable parental anxiety and are a frequent cause of referral to paediatric services. This report is of a family of seven siblings all of whom have suffered breath-holding spells, including three who developed breath-holding spells within the neonatal period, with the other four developing them at 3–4 months of age. All of the children have on occasions exhibited convulsive activity at the termination of the episode. All had normal initial electroencephalogram's (EEG) and one had centrotemporal spikes on his EEG when repeated at age 6 years. Anticonvulsant therapy resulted in a reduced frequency of breath-holding spells. The epidemiology, pathophysiology and therapy of breath-holding spells is discussed with reference to this unique family. This report gives further credence to the notion that there often may be a familial predisposition to breath-holding spells.

Facial paraesthesia due to perineural malignant infiltration is a well recognised complication of basal and squamous cell carcinomas of the head and neck. Perineural involvement was originally attributed to involvement of the perineural lymphatics; however subsequent studies have demonstrated conclusively that these lymphatics do not exist and that the invasion occurs along the line of least resistance. Previous studies on perineural spread of carcinomas of the head and neck have emphasised diagnostic biopsy of an involved nerve (e.g. the infraorbital, mental or major branches of the trigeminal nerve), or at times craniectomy with exploration of the gasserian ganglion. We suggest that in many cases the diagnosis can be obtained by biopsy of the anaesthetic skin alone, without recourse to more involved biopsy techniques. The following case report illustrates this point.

Severe spasticity is a major problem in the rehabilitation of patients with dysfunction of the spinal cord or cerebral hemispheres. Oral baclofen is often effective. However, in patients with severe spasticity adequate control may not be obtained from oral therapy with the drug. Over the past 5 years we have developed a program for the use of intrathecal baclofen for severe spasticity, and in relation to this discuss patient assessment, practical aspects of drug administration, complications of therapy and patient benefits. Continuous intrathecal baclofen is a safe and effective adjunct to physical therapy in the management of patients with severe spasticity.

We have prospectively studied 45 patients undergoing scoliosis surgery (48 procedures) for evidence of postoperative acute radiculopathy. Posterior spinal fusion was performed in 42 patients (Cotrel Dubousset 28, Harrington rod with wires 9, Hartshill rectangles 5); anterior spinal fusion in 5 (Webb Morley) and an anterior release procedure in 5. Fourteen patients (29%) had sensory and/or motor signs of radiculopathy post-operatively, with moderate to severe symptoms in 10 and mild symptoms in 4. The radiculopathies were considered traumatic in 7 patients, in whom radiculopathy correlated with placement of a hook or passage of a sublaminal wire. In the remaining 7 patients, traction was considered the likely mechanism of injury; in these there was a significant association with the degree of postoperative correction of the scoliosis where it was substantially beyond the preoperatively demonstrated flexible range (p = 0.008). A system of intraoperative electromyographic monitoring for possible prevention of this complication is described. Radiculopathy is a common complication of scoliosis surgery.

Zeta waves are a distinctive form of sharply contoured biphasic delta waves that have been associated with underlying structural lesions. We have prospectively interpreted the EEGs of 840 consecutive patients blinded for clinical details. Thirty three patients had zeta waves in at least one recording and 87% of these had an underlying structural lesion on neuroimaging. By excluding those with bifrontal intermittent rhythmic delta activity and bifrontal zeta waves, the positive predictive value of zeta waves for an underlying structural lesion increases to 96%. We conclude that zeta waves are distinctive and easily recognisable delta waves which are highly predictive of recent or residual cerebral damage from a variety of causes, including cerebral trauma and infarction.

We report a 35-year-old woman who developed herpes simplex virus (HSV) type 1 interstitial nephritis following a cadaveric renal transplant. Transplant function was poor and a transplant nephrectomy was performed 23 days post-transplant. Histological changes characteristic of herpes virus infection were seen on the renal biopsy with positive immunoperoxidase staining for HSV. HSV 1 was cultured from the transplant nephrectomy specimen.

A patient with delayed episodes of extreme bradycardia, asystole and syncope occurring 5 to 9 weeks after traumatic high cervical spinal cord injury is described. Temporary transvenous ventricular pacing followed by oral propantheline was required to prevent further episodes. The investigation, physiology and treatment of this arrhythmia in tetraplegia are discussed.

OBJECTIVE To report a case of central and extrapontine myelinolysis with unusual behavioural manifestations that developed after slow (not more than 0.5 mmol sodium per litre per hour) correction of hyponatraemia. CLINICAL FEATURES A 51-year-old Caucasian woman with hyponatraemia caused by psychogenic polydipsia experienced a delayed onset of behavioural changes with some ataxia, but no pyramidal signs, after correction of the hyponatraemia. INTERVENTION AND OUTCOME The hyponatraemia was corrected with a combination of hypertonic saline and fluid restriction at the currently recommended rate of not more than 0.5 mmol of sodium per litre per hour. CONCLUSION Central and extrapontine myelinolysis may develop after slow correction of hyponatraemia. Behavioural manifestations may be the most prominent clinical feature.

Ophthalmoplegia is a rarely observed sign in carbamazepine and other anticonvulsant overdoses. We present a patient who developed transient complete external ophthalmoplegia and asterixis with relative preservation of consciousness, in association with carbamazepine toxicity. Previously reported cases and proposed mechanisms are reviewed. (Aust NZ J Med 1991; 21: 886–887.)

Orbital myositis implies orbital inflammation confined to one or more of the extraocular muscles. Orbital computerised tomography (CT) demonstrates irregular extraocular muscle enlargement which extends anteriorly to involve the tendon (muscle insertion). Six cases of presumed orbital myositis are reported, in each of whom the diagnosis was suspected clinically and confirmed by the orbital CT scan appearances. The mean age of the patients was 33 years (range 8-45 years). All presented with painful ophthalmoplegia and the majority manifested proptosis (five cases), conjunctival congestion (five cases) and periorbital and eyelid edema (two cases). Systemic corticosteroid therapy was used in two patients initially and also in another patient who relapsed, with rapid and dramatic responses. Extraocular muscle biopsy was performed in one case, disclosing features of non-specific muscle inflammation and no evidence of vasculitis. It is considered that orbital myositis is a discrete, identifiable subgroup within the spectrum of the nonspecific idiopathic orbital inflammatory syndromes; termed previously orbital 'pseudotumours'. Although the clinical features are frequently suggestive, they are nonspecific, and non-invasive investigations such as orbital ultra-sonography and CT scanning are required for precise anatomical tissue localisation and diagnosis. The role of ocular muscle biopsy is probably limited to atypical cases, or those unresponsive to steroid therapy, particularly to exclude neoplasia. Orbital myositis may be acute, subacute or recurrent. The acute form responds well to high doses of oral corticosteroids tapered gradually, but it may recur or become chronic. The subacute form of the disease responds less well.

Purpose Impaired GABAergic inhibition has been implicated in the pathophysiology of epilepsy. The possibility of a paradoxical excitatory effect of GABA in epilepsy has been suggested, but has not been investigated in vivo . We investigated pre- and post-synaptic GABAergic mechanisms in patients with idiopathic generalised epilepsy (IGE). Method In 10 patients and 12 control subjects we explored short- and long-interval intracortical inhibition (SICI, LICI; post-synaptic GABA A and GABA B -mediated respectively) and long-interval intracortical facilitation (LICF; pre-synaptic disinhibition) using transcranial magnetic stimulation. Results While post-synaptic GABA B -mediated inhibition was unchanged in IGE ( p =0.09), LICF was reduced compared to controls (controls: 141±17% of baseline; untreated patients: 107±12%, p =0.2; treated patients: 79±10%, p =0.003). GABA A -mediated inhibition was reduced in untreated patients (response amplitude 56±4% of baseline vs. 26±6% in controls, p =0.004) and normalised with treatment (37±12%, p =0.5 vs. controls). When measured during LICI, GABA A -mediated inhibition became excitatory in untreated IGE (response amplitude 120±10% of baseline, p =0.017), but not in treated patients. Conclusion Pre- and post-synaptic GABA-mediated inhibitory mechanisms are altered in IGE. The findings lend in vivo support to evidence from experimental models and in vitro studies of human epileptic brain tissue that GABA may have a paradoxical excitatory role in ictogenesis.

Benign headaches related to sexual activity and exertion are being recognised with increasing frequency. We wish to report a case of benign sexual headache (Type 2) and benign exertional headache, occurring sequentially in the same patient. Multiple areas of cerebral arterial spasm were demonstrable on angiography. This observation would support the concept that benign sexual headache (Type 2) and benign exertional headache may have a similar pathophysiology.

Primary position upbeating nystagmus has been associated clinically with intra-axial brainstem and cerebellar lesions but evidence for more precise localisation to the ponto-mesencephalic and ponto-medullary junctions is accumulating. We report the occurrence of primary position upbeating nystagmus in three patients who had clinical signs of pontine lesions at the ponto-mesencephalic and ponto-medullary junctions. Radiological confirmation was possible in two cases.