A 52-year-old woman was referred for a progressive neurological condition which started a year before with continuous irregular twitching of the right facial and arm muscles as well as the tongue and palate, followed by progressive dysphagia, right hemiparesis, ataxia, dysphasia and dysarthria. Though magnetic resonance imaging (MRI) at clinical presentation and a year after were both normal (Figure A1), Rasmussen's encephalitis (RE) was strongly suspected and treatment with corticosteroids and immunoglobulins were begun. A third MRI, two years after onset, revealed mild T2 hyperintense subcortical white matter changes over the left perisylvian region (Figure A) which confirmed our initial suspicion of RE as she now met clinical, electrophysiological and morphological criterias for RE. While waiting for a cerebral biopsy after unsatisfactory response from antiepileptic drugs, corticosteroids and immunoglobulins, her condition markedly worsened less than three years after onset with the sudden occurrence of status epilepticus requiring intubation and continuous infusions of midazolam and propofol.

An eight-month-old male Caucasian infant presented with ataxia and titubations, which had been noticed shortly after birth. He was born to healthy non-consanguineous parents after an unremarkable pregnancy. There was no maternal use of drugs, alcohol or tobacco. A prenatal ultrasound at 36 weeks conceptual age (performed at the request of the parents since the 20 week ultrasound had not been performed) revealed an enlarged posterior fossa, no cerebellar tissue, a normal corpus callosum and no evidence of hydrocephalus. He was delivered via spontaneous vaginal delivery at 37 weeks gestation without complications. Birth weight was 3630g and the neonatal course was unremarkable. Developmentally, at eight months-of-age he could not sit. A formal developmental assessment at 19 months-of-age revealed gross and fine motor delay. He was pulling to stand and was cruising but was not walking independently. He was able to stack two cubes. He was very social, highly imitative and used over 50 words. His words were clear and there was no dysarthria. His receptive and expressive language skills were deemed to be at the 18-21 month level. Family history was non-contributory. Physical examination at 19 months-of-age revealed weight and height between the 10-25 percentiles and head circumference at the 25th percentile. Head titubation was present throughout the examination. Extraocular movements were full, with bilateral intermittent esotropia. Upon fixing of the head, horizontal nystagmus and saccadic intrusions on smooth pursuit exam were noted. Fundoscopic examination was normal. He had mild truncal hypotonia, with appropriate strength for his age.

A previously healthy ten-year-old girl was involved in a high speed motor vehicle accident (MVA) in which she was the belted front-seat passenger. The patient's teeth marks on the dashboard were evidence of a high-velocity impact. Her Glasgow Coma Score on scene was 13, and she was amnestic for the event. She was subsequently transported to the emergency room in full spinal precautions; on arrival she was hemodynamically stable with a Glasgow Coma Score of 14, complaining of neck and jaw pain. Neurological examination revealed impaired abduction of the right eye, with no other focal deficits. She had oral lacerations and bruising over the mandibles bilaterally.

Computed tomogram (CT) scan of the head was initially interpreted as normal, but on closer inspection demonstrated a 4mm retroclival hematoma (Figure 1). Sagittal CT through the upper cervical spine revealed the hematoma was epidural, bounded by the spheno-occipital synchondrosis superiorly and by the mid-body of the axis inferiorly (Figure 2). The odontoid was retroflexed (Figure 2). Bilateral mandibular fractures were also uncovered on facial imaging.

A 74-year-old man presented with a four week history of behavioural disturbances, upper and lower extremity numbness and impaired balance. He had been treated with metronidazole for six months for osteomyelitis of the right hallux. Examination revealed encephalopathy, and glove-and-stocking sensory loss to pinprick with reduced vibration threshold at the toe. The gait was wide based and ataxic. Nerve conduction studies showed a large fibre sensory-motor axonal polyneuropathy. Magnetic resonance imaging (MRI) revealed a solitary restricted diffusion lesion in the splenium of the corpus callosum (Figure A, B) with subtle prolongation of T2 (Figure C). The radiographic differential diagnosis included hypoglycaemia, viral encephalitis, antiepileptic drug toxicity/withdrawal and metronidazole toxicity. The combination of the imaging finding with the history of prolonged metronidazole use suggested metronidazole induced encephalopathy.

A 78 year-old woman presented with acute onset low back pain with radiation into the right T12-L2 dermatomes, progressive flaccid paraparesis, urinary incontinence and bilateral lower extremity paresthesias. Examination revealed flaccid paraparesis, and a T12 sensory level to pin with intact vibration and proprioception. Magnetic resonance imaging (MRI) (Figure 1) of the spinal cord demonstrated T2 hyperintensity and restricted diffusion from T12 to the conus medullaris. Computed tomogram (CT) aortogram (Figure 2) highlighted an ulcerated plaque and thrombus at the approximate level of the artery of Adamkiewicz. These findings were consistent with a spinal cord infarct of the cord from T12-L2. The patient was treated with Clopidogrel and IV heparin (x two days) and was transferred for spinal cord rehabilitation.

A previously healthy five year-old boy was seen after intermittent strangulation attempts over the course of two days. Details of the event are vague due to lack of reliable adult witnesses. There was no indication of toxic exposure. General examination on arrival to the emergency department revealed an alert boy with bruising of the neck consistent with multiple strangulation attempts. There was no evidence of heart, kidney, or liver involvement to suggest systemic hypoperfusion or organ failure. Investigations done on arrival showed no acidosis, and a capillary blood gas 48 hours later revealed a normal carboxyhemoglobin. Although the initial neurologic exam was near normal, severe generalized dystonia developed over the next four weeks, requiring intrathecal baclofen treatment.

A 34 year-old female without prior relevant medical history presented to our emergency room with a two-day history of neck pain, odynophagia and elevated body temperature up to 38.2° C. Her general practitioner had started the patient on antibiotic treatment with ciprofloxacin and referred her to our emergency department for further diagnostic workup and treatment of suspected meningitis. Initial neurological examination revealed neck rigidity and head pain without further focal neurological signs. Body temperature was 37.7 °C, blood analyses revealed a normal leukocyte count (8.900/μl) and normal C-reactive protein (<0.3mg/dl), blood cultures were sterile. Lumbar puncture was without pathological findings (<1 leukocytes/μl, normal levels for glucose, lactate and protein). Cervical magnetic resonance imaging could rule out osseous injury and cervical myelopathy, however a small prevertebral, retropharyngeal fluid collection was visible (Figure 1a-c). This prompted the diagnosis of acute retropharyngeal calcific tendinitis (RCT). This diagnosis was confirmed by conventional x-ray showing the presence of a characteristic amorphous calcification in the retropharyngeal space anterior to the C1-C2 segments (Figure 1d). Treatment with i.v. methylprednisolone (250mg) was started and pain was reduced shortly after the first infusion. The patient was discharged on tapered oral methylprednisolone and non-steroidal anti-inflammatory drug (NSAID) treatment. Symptoms resolved completely within a week.