21 Neurological disease
Questions
Please what is (are) the likely cause(s) of sudden sharp but brief pain (resembling pin prick) in the right lower abdomen?
Is bilateral VIth cranial nerve palsy always a false-localizing sign (i.e. does it indicate an increased intracranial pressure and not pathology of the nerves or their nuclei)?
Can the Brown-Séquard syndrome be diagnosed with pyramidal weakness of one lower limb and hypoaesthesia of the other lower limb but with no dissociative sensory loss of the hypoaesthetic limb?
I have seen many established ischaemic stroke patients with CT-documented capsular infarction and hemi-hypotonia despite exaggerated reflexes. How would you explain the hypotonia? Could it be due to a corticorubral fibre lesion?
There seems now to be a consensus about starting aspirin therapy in acute ischaemic strokes as early as possible. Why has this changed from past recommendations to avoid aspirin early (during the first 48 hours) during the ischaemic stroke on the pretext that it could convert an ischaemic infarct into a haemorrhagic one, thus increasing the dangers of complications like cerebral oedema and raised intracranial pressure? If both opinions are based on clinical trials, what is the significance of the much hyped ‘evidence-based medicine’?
I read recently that hyperuricaemia has something to do with stroke? Is it recommended to give allopurinol to stroke patients irrespective of their serum uric acid?
What are the causes of epilepsy with a normal electroencephalogram (EEG), other than metabolic causes? Could epilepsy due to CNS causes be associated with a normal EEG? Could epilepsy due to the gradual withdrawal of an antiepileptic drug occur as much as 1 year later?
How often can drop attacks with loss of consciousness be due to atonic fits in the absence of any other type of fit?
What anti-epileptic drug is recommended for a child with epilepsy and co-morbid attention deficit hyperactivity disorder (ADHD)? Can Ritalin safely be used for treatment?
Is valproate effective if given rectally in status epilepticus and, if so, what dose is recommended?
Does a lesion of Guillain-Mollaret’s triangle in the brain stem cause a type of myoclonus other than symptomatic palatal myoclonus?
Does hemiplegia due to multiple sclerosis present with hemiparesis rather than dense hemiplegia (which is more characteristic of a stroke)? Other than age, what are the clinical signs that would help differentiate between the two?
What is the role of anticonvulsants in a case of encephalitis and how long should one continue them?
Should you treat a patient who has a brain cysticercosis lesion? The text seems to say ‘Yes’ but there is great uncertainty about it.
Also, should one ‘worm’ the patient’s gut when you find brain lesions; if so, with what?
In the case of anterior spinal artery occlusion, can the patient have intact sensations in the lower limbs?
Can the creatine phosphokinase (CPK) level in the blood, or the presence of certain auto-antibodies, help to differentiate muscle dystrophies from myositis?
What is the recommended target of total and low-density lipoprotein (LDL) cholesterol in secondary prevention of ischaemic stroke?
Are the pathological terms ‘neurinoma’ and ‘schwannoma’ interchangeable? Do these differ from neurofibroma as some neurology textbooks do not differentiate between these terms and seem to apply the terms neurinoma and neurofibroma interchangeably to spinal nerve tumours arising from neurilemmal sheaths?
Sharp brief pains often occur for no known reason. Nerve entrapment is said to be one cause, without much evidence.
The VIth nerve nucleus sends axons directly into the VIth nerve to supply the lateral rectus, and also into the contralateral medial longitudinal fasciculus and up into the IIIrd nerve nucleus where they synapse with neurones from the medial rectus. Damage to the VIth nerve nucleus prevents both eyes moving ipsilaterally. A bilateral VIth nerve palsy is always a false localizing sign.
Yes, trigeminal neuralgia can occur in, for example multiple sclerosis and tumours of the 5th nerve.
Taste is not affected in supranuclear lesions (i.e. upper motor neurone lesions). Involvement of the facial nerve proximal to the origin of the chorda tympani will cause loss of taste. Lesions beyond the stylomastoid foramen will not affect taste.
The weakness often starts distally, e.g. the hands, but then spreads to involve forearms, the biceps and triceps followed by shoulder muscles.
Wallenberg, in his original description of the lateral medullary infarction syndrome, did not include diplopia. Diplopia does occur; remember that the VIth nerve is very near to the Vth nerve nucleus.
Patients with a carotid artery dissection are often treated with anticoagulants despite the underlying bleeding into the vessel wall. As the blood enters the wall of the artery the lumen becomes progressively narrowed and thrombosed. It is to try to prevent further thrombosis and emboli occurring that anticoagulants are given.
There are a few well-constructed randomized controlled trials (RCTs) in this condition. Heparin is given in standard doses but the evidence for its value is small. It is followed by warfarin and heparin is stopped when the international normalized ratio is in the target range of 2.5.
There is no one drug in this situation. It partly depends on the type of epilepsy. Any drug must be used carefully. Either valproate or ethosuximide is a reasonable choice but both are associated with hyperactivity. Do not use Ritalin.
Central tegmental olivary lesions occur which can be the result of vascular, neoplastic or traumatic injury. Symptomless palatal myoclonus is rare; no other type of myoclonus occurs with this lesion.
A quick search reveals no studies of low blood levels of vitamin D (25-hydroxycholecalciferol) and relapse in MS, but the Multiple Sclerosis Society (http://www.mssociety.org.uk), might be able to help.
There have been many studies, with an impression that the risk of a relapse of the disease is slightly increased in pregnancy, particularly in the puerperium. There is no evidence that pregnancy affects the long-term prognosis, and most clinicians no longer advise against pregnancy.
No exact figures are easily available as frequency depends, for example, on which country, co-infection with HIV and many other factors. TB meningitis is, however, quite a common cause of meningitis and must always be high on the list of possible causes.
Any seizures that occur in a patient with encephalitis will need treatment which should be continued for approximately 3 months although there is no firm evidence on the time frame.
The exact existence of normal pressure hydrocephalus, as a true separate entity from dementia, has been questioned. The classic clinical triad is as you have described. MR shows ventriculomegaly but this is also seen in dementia.
Digoxin has been used but there is little data for its use. Acetazolamide 250 mg × 4 daily, increasing to 500 mg and then 1 g × 4 daily (if tolerated) is the preferred choice.
Electromyographic studies show continuous motor activity in the paraspinal muscles in the stiff person syndrome and not in Isaac’s syndrome.
You can’t make the diagnosis without papilloedema. CSF pressure measurement is usually performed but repeat lumbar puncture with removal of fluid is used as a treatment.
Above 200 mg/dL is high and attempts should be made to reduce this level with lifestyle changes and dietary modifications. Elevated serum triglyceride levels are an independent risk factor for the development of atherosclerosis. The data on whether raised triglycerides are a risk factor for ischaemic stroke are, however, poor.
