Case histories: Answers

Published on 09/04/2015 by admin

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Case histories

Answers

Case 1: Carpal tunnel syndrome (p. 106)

The history of numbness in the hands waking the patient from sleep is classical for carpal tunnel syndrome. As the median nerve compression progresses, the symptoms intrude into the day and a fixed deficit in median nerve distribution may emerge. Nerve conduction studies usually confirm the diagnosis and treatment is with decompression at the wrist.

Case 2: Acute bacterial meningitis (p. 98)

The fever points to infection and the neck stiffness suggest meningitis. The time course is typical for acute bacterial meningitis, which may be complicated by seizures. Seizures are commoner in encephalitis but the evolution is usually slightly slower in onset and there is less neck stiffness. He should be treated with antibiotics prior to having a scan and lumbar puncture.

Case 3: Myasthenia gravis (p. 110)

The variability in the history, fatiguability and a pattern of diplopia not fitting with any specific cranial nerve make the diagnosis highly likely to be myasthenia gravis. Diagnostic tests are acetylcholine receptor antibodies, neurophysiology and edrophonium test. Treatment is with pyridostigmine and immunosuppression.

Case 4: Juvenile myoclonic epilepsy (p. 74)

The history of myoclonic jerks for many years before a tonic-clonic seizure is typical and many patients also have absences. This form of epilepsy is often made worse by carbamazepine and the most effective treatment is usually sodium valproate.

Case 5: Benign paroxysmal positional vertigo (BPPV) (p. 47)

This is the typical history for BPPV and the manoeuvre described is Hallpike’s test, which confirms the diagnosis. Treatment is the Epley’s manoeuvre.

Case 6: Subdural haematoma (SDH) (pp. 67 and 78)

The history and signs point to a progressive left hemisphere lesion. With a head injury preceding the onset, the first diagnosis is SDH. These are commoner in patients on warfarin or aspirin. Alternative diagnosis is a tumour unrelated to the injury.

Case 7: Cervical cord compression (p. 80–83)

He has lower limb spasticity due to bilateral upper motor neurone dysfunction pointing to a spinal lesion. The highest abnormal sign is the absent biceps reflexes, implying a lower motor neurone abnormality at the level of the biceps motor roots and therefore a motor level at C6. Worsening with cough suggests the cause is compressive; spondylosis or tumour. He should have emergency MRI of the cervical spine and neurosurgical referral.

Case 8: Guillain–Barré syndrome (GBS) (p. 104)

The patient has generalized weakness and loss of reflexes pointing to a diffuse lower motor neurone disturbance and the patient has a sensory disturbance consistent with a neuropathy. The subacute course and preceding infection are typical of GBS. Nerve conduction abnormalities and elevated protein level in the cerebrospinal fluid are common but may take time to develop; treatment is with IV immunoglobulin or plasmaphoresis on the basis of the clinical picture.

Case 9: Migraine and analgesic misuse headache (p. 43)

The earlier history of discrete headaches is typical of migraine. This has changed to a more continuous headache only partially treated by analgesia, typical of analgesic misuse headaches. Common culprits are codeine, caffeine, paracetamol and triptans. No investigation required. Treatment is to withdraw analgesia and consider migraine prophylaxis.

Case 10: Syncope (p. 44)

People who faint often try first to get out into fresh air. The history of passing out again when she tried to get up is also typical. Most faints are associated with some limb twitching and this does not mean they have had a seizure. Most cases in healthy young individuals require no investigation, but recurrent or atypical episodes may merit ECG, 24-h ECG, tilt testing or echocardiography.

Case 11: Left carotid territory transient ischaemic attack (TIA) (pp. 70–71)

The tempo points to a TIA and the speech disturbance puts it into carotid artery territory. He should have Doppler carotid arteries and receive aspirin. He is mildly hypertensive and other vascular risk factors should also be addressed and treated.

Case 12: Ulnar neuropathy (pp. 106–107)

The distribution of weakness and numbness are typical of ulnar neuropathy. Investigation is with nerve conduction studies, which usually show conduction delay across the elbow due to compression. Conservative treatment is sometimes effective but surgical decompression or transposition may be required.

Case 13: Multiple sclerosis (MS) (pp. 19 and 84–87)

The earlier history and signs in her right eye are typical of previous optic neuritis. The new signs are of a left internuclear ophthalmoplegia and ataxia, which both indicate a lesion in the brain stem. Thus, she has lesions disseminated in time (now and some years ago) and place (the optic nerve and brain stem) making a clinical diagnosis of MS. Investigations are MRI brain, sometimes lumbar puncture and visual evoked potentials and blood tests to exclude rare mimics of MS, where indicated.

Case 14: Parkinson’s disease (PD) (pp. 88–91)

Reduced arm swing is a typical early symptom of PD. Stiffness may lead the condition to be mistaken for a rheumatological disorder. The other symptoms and signs are also typical. One-third of patients have no tremor at presentation. There are no diagnostic investigations, but a careful history and examination may help to exclude other, rarer Parkinsonian syndromes.

Case 15: Motor neurone disease (amyotrophic lateral sclerosis, ALS) (pp. 108–109)

Widespread fasciculations and wasting point to a diffuse lower motor neurone disturbance including bulbar muscles. The brisk reflexes and upgoing plantars indicate an upper motor neurone lesion. She has no sensory signs. Thus, she demonstrates mixed upper and lower motor neurone involvement in multiple regions, typical of ALS. The progressive course is typical. Nerve conduction studies and EMG will provide support for the diagnosis and exclude mimics.

Case 16: Subarachnoid haemorrhage (SAH) (pp. 72–73)

Any sudden-onset headache, especially during exertion, is SAH until proven otherwise. The duration is rather long for benign exertional headaches, which have also usually occurred several times by presentation. A CT scan is normal in about 10% of SAH and a lumbar puncture with spectrophotometry for haemoglobin breakdown products is needed to exclude the diagnosis.

Case 17: Left hemisphere tumour (p. 94)

The symptoms and signs point to an upper motor neurone lesion, and with the associated speech disturbance this is likely to be in the left cerebral hemisphere. The progressive time course makes a tumour the most likely cause. The jerking episodes are focal seizures followed by ‘Todd’s paresis’. Investigation with CT or MRI and a screen for primary tumours, including chest X-ray, ultrasound or CT of the abdomen, blood count, renal and liver function are indicated. Rarer causes include cerebral abscess or chronic subdural haematoma. He should be treated with an antiepileptic drug such as carbamazepine. If a tumour is found, then corticosteroids may be indicated prior to surgery/biopsy.

Case 18: Left vertebral artery dissection (pp. 64–69)

The physical signs include a left Horner’s syndrome and left 6th nerve palsy. These are in the brain stem above the decussation of the descending pathways, explaining the right hemiparesis and sensory loss, and involvement of the ipsilateral cerebellar pathways explains the ipsilateral ataxia. The acute onset is typical of a stroke. The history of neck trauma and pain suggests dissection of the left vertebral artery. Arterial dissection is the commonest identifiable cause of stroke in young adults and pain over the vessel preceding infarction is typical. Investigation is with specially tailored MRI. Optimal treatment is not established; either aspirin or anticoagulation.

Case 19: Cardioembolic stroke (pp. 64–69)

The signs are of a right hemiparesis and the sudden onset points to a vascular cause. In a patient with atrial fibrillation, embolism of a cardiac thrombus is likely, but the history of previous rheumatic fever also raises the rarer possibility of infective endocarditis. He should have CT scan, Doppler carotids, echocardiogram, with erythrocyte sedimentation rate (ESR), C reactive protein (CRP) and blood cultures if there is any suggestion of infection. If there is no alternative cause, he should receive long-term warfarin.

Case 20: Alzheimer’s disease (AD) (pp. 54–55)

He has a slowly progressive memory disturbance affecting episodic and visuospatial memory (bihemispheric disturbance) with alteration of personality and no physical problems; the typical picture of AD. Investigation is with CT/MRI, renal and liver function, thyroid function, blood count, ESR and syphilis serology.

Case 21: Sporadic Creutzfeldt–Jakob disease (CJD) (pp. 55, 99)

This is the typical history of sporadic CJD with rapidly progressive dementia, ataxia and startle-sensitive myoclonic jerks. MRI brain may show increased signal in the basal ganglia or thalamus and EEG may show characteristic periodic complexes. There is no absolute antemortem diagnostic test and no specific treatment. Management is supportive.

Case 22: Giant cell arteritis (GCA or temporal arteritis) (p. 40)

GCA is the most important diagnosis to consider in elderly patients with recent-onset headaches. The clinical features of this case are classical but are not always present. Over 90% have either a raised ESR or CRP in the blood and a temporal artery biopsy is usually diagnostic. Treatment with high-dose corticosteroids should be instituted as soon as the diagnosis is suspected and a biopsy should be undertaken within a few days.

Case 23: Focal epilepsy (pp. 74–79)

These are typical focal seizures of temporal lobe origin. MRI brain and EEG are required but may be normal and, as she has had multiple episodes, she needs antiepileptic treatment; carbamazepine would be the most commonly used drug. She should be advised not to drive and to inform the DVLA and her insurance company, and advised regarding avoiding situations that would put her or others at risk if she were to have a seizure. She should be informed about the risk of carbamazepine interacting with the oral contraceptive and warned regarding teratogenicity.

Case 24: Tuberculous meningitis (TBM) (pp. 97 and 38)

Headache and neck stiffness with fever suggest an infective meningeal process. Infarction of facial and vestibulocochlear nerves and mild hydrocephalus on CT scan are due to inflammation of the basal meninges. The subacute onset, with symptoms coming over weeks, with weight loss and multiple cranial nerve lesions are typical of TBM. The next test is CSF analysis by lumbar puncture if considered safe from CT scan appearances, or by cisternal puncture if not. Treatment is 1 year of antituberculous therapy guided by organism sensitivities. Underlying HIV needs to be considered.

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Case histories

Answers

Case 1: Carpal tunnel syndrome (p. 106)

The history of numbness in the hands waking the patient from sleep is classical for carpal tunnel syndrome. As the median nerve compression progresses, the symptoms intrude into the day and a fixed deficit in median nerve distribution may emerge. Nerve conduction studies usually confirm the diagnosis and treatment is with decompression at the wrist.

Case 2: Acute bacterial meningitis (p. 98)

The fever points to infection and the neck stiffness suggest meningitis. The time course is typical for acute bacterial meningitis, which may be complicated by seizures. Seizures are commoner in encephalitis but the evolution is usually slightly slower in onset and there is less neck stiffness. He should be treated with antibiotics prior to having a scan and lumbar puncture.

Case 3: Myasthenia gravis (p. 110)

The variability in the history, fatiguability and a pattern of diplopia not fitting with any specific cranial nerve make the diagnosis highly likely to be myasthenia gravis. Diagnostic tests are acetylcholine receptor antibodies, neurophysiology and edrophonium test. Treatment is with pyridostigmine and immunosuppression.

Case 4: Juvenile myoclonic epilepsy (p. 74)

The history of myoclonic jerks for many years before a tonic-clonic seizure is typical and many patients also have absences. This form of epilepsy is often made worse by carbamazepine and the most effective treatment is usually sodium valproate.

Case 5: Benign paroxysmal positional vertigo (BPPV) (p. 47)

This is the typical history for BPPV and the manoeuvre described is Hallpike’s test, which confirms the diagnosis. Treatment is the Epley’s manoeuvre.

Case 6: Subdural haematoma (SDH) (pp. 67 and 78)

The history and signs point to a progressive left hemisphere lesion. With a head injury preceding the onset, the first diagnosis is SDH. These are commoner in patients on warfarin or aspirin. Alternative diagnosis is a tumour unrelated to the injury.

Case 7: Cervical cord compression (p. 80–83)

He has lower limb spasticity due to bilateral upper motor neurone dysfunction pointing to a spinal lesion. The highest abnormal sign is the absent biceps reflexes, implying a lower motor neurone abnormality at the level of the biceps motor roots and therefore a motor level at C6. Worsening with cough suggests the cause is compressive; spondylosis or tumour. He should have emergency MRI of the cervical spine and neurosurgical referral.

Case 8: Guillain–Barré syndrome (GBS) (p. 104)

The patient has generalized weakness and loss of reflexes pointing to a diffuse lower motor neurone disturbance and the patient has a sensory disturbance consistent with a neuropathy. The subacute course and preceding infection are typical of GBS. Nerve conduction abnormalities and elevated protein level in the cerebrospinal fluid are common but may take time to develop; treatment is with IV immunoglobulin or plasmaphoresis on the basis of the clinical picture.

Case 9: Migraine and analgesic misuse headache (p. 43)

The earlier history of discrete headaches is typical of migraine. This has changed to a more continuous headache only partially treated by analgesia, typical of analgesic misuse headaches. Common culprits are codeine, caffeine, paracetamol and triptans. No investigation required. Treatment is to withdraw analgesia and consider migraine prophylaxis.

Case 10: Syncope (p. 44

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