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In patients with pre-existent cervical spinal canal stenosis, minimal trauma, leading to neck hyperextension, can cause a significant increase of spinal cord compression. However, spinal cord injury is generally associated with major trauma and is usually not expected in patients with minor trauma. The resulting symptoms are diverse, making it even more difficult to diagnose. To illustrate the variety in symptoms at presentation, we describe two male patients aged 66 and 69. Rapid diagnosis is important as acute neurosurgical intervention may be indicated. Physical neurological examination, and in particular testing peripheral reflexes, can contribute to the rapid diagnosis of spinal cord injury. Cervical spine CT should not only be assessed for acute traumatic injury, but also for possible stenosis of the cervical spinal canal.

A young, non-obese woman aged 24 years with normal blood pressure developed intracranial hypertension after the oral use of tetracycline. Neuro-ophthalmologic examination revealed severely reduced acuity, papilledema, and concentric impaired visual fields. She was treated with acetazolamide and recurrent lumbar punctures and recovered, but without improvement in either acuity or visual fields. Intracranial hypertension is a fairly rare disease characterised by increased intracranial pressure without structural abnormalities in the brain or hydrocephalus, and is termed idiopathic in the absence of an underlying cause. Tetracycline should be considered as a cause of intracranial hypertension if a patient complains of previously unknown headache a few days after its ingestion. Headache and the presence of bilateral papilledema, decreased visual acuity and visual-field defects are indications for urgent referral to a neurologist. Therapy consists of a combination of repetitive lumbar punctures and medication. Surgical interventions include lumboperitoneal shunting and optic nerve fenestration. Intracranial hypertension may lead to irreversible decreased visual acuity and visual-field defects resulting in disability.

A 24-year-old woman of Somali origin delivered at term after an uncomplicated pregnancy. Post-partum haemorrhage resulted in hypovolaemic shock which was treated by hysterectomy. Five days later she became comatose due to unrecognised hypoglycaemia which caused severe irreversible brain damage and status epilepticus. Treatment in the intensive care unit with artificial respiration, prednisolone, desmopressin, inotropic support, barbiturates and an anaesthetic under EEG guidance was unsuccessful. The patient died 28 days post-partum. The hypoglycaemia was due to a combination of (a) inadequate glucose intake and (b) lack of counter-regulatory mechanisms due to a deficiency of steroids and growth hormone as a result of loss of pituitary function (Sheehan syndrome) together with adrenocortical insufficiency. The combination of Sheehan syndrome and primary adrenocortical insufficiency has not been described previously in the literature.