Discover millions of ebooks, audiobooks, and so much more with a free trial

Only $11.99/month after trial. Cancel anytime.

Case Presentations in Neurology
Case Presentations in Neurology
Case Presentations in Neurology
Ebook604 pages

Case Presentations in Neurology

Rating: 0 out of 5 stars

()

Read preview

About this ebook

Case Presentations in Neurology presents a selection of case histories demonstrating how patients with often quite simple problems may present and to bring out aspects of their diagnosis and management. All the patients presented to the Department of Neurology including those with more obscure diagnoses. The book consists of 12 exercises, each of six cases broadly corresponding to the style of the MRCP (UK) written case history papers. Each case is set out with the history and physical findings given first. There follows either a series of questions or true/false statements on one side of the page which the reader should attempt before continuing on to the answer section on the other side. There then follows a short discussion about each case and a single reference. This book is intended for those doctors studying for higher professional qualifications such as the MRCP, although it may be of interest and use to medical students approaching their final examinations.
LanguageEnglish
Release dateOct 22, 2013
ISBN9781483141305
Case Presentations in Neurology

Related to Case Presentations in Neurology

Wellness For You

View More

Related categories

Reviews for Case Presentations in Neurology

Rating: 0 out of 5 stars
0 ratings

0 ratings0 reviews

What did you think?

Tap to rate

Review must be at least 10 words

    Book preview

    Case Presentations in Neurology - G. S. Venables

    potential

    Exercise 1

    Case 1.1

    An impotent man

    Publisher Summary

    This chapter discusses the medical case of an impotent man. A 32-year-old man sought medical advice because of impotence. He had been married for 8 years and had two children aged 6 and 4 years. Previous sexual activity had been satisfactory. Two months before seeking advice, he had developed total failure of erection and ejaculation, but claimed that sexual desire was undiminished. On direct questioning, it was learnt that there were no morning erections and he had experienced frequency of micturition for 6 months and urgency for 2 months. On two or three occasions during the previous 6 months, he had noticed a tendency to constipation. He was a healthy male with no abnormality on general examination including the genitalia. Neurological examination revealed normal tone and power in all four limbs, but the tendon stretch reflexes were brisk. Impotence is commonly of psychological origin. The combination of impotence with bladder and bowel dysfunction suggests an organic neurological cause. Anatomically, this may be attributable to a lesion in the parasympathetic nerve supply to the bladder, bowel, and sexual organs, or secondary either to spinal cord, to cauda equina disease, or to an autonomic or generalized peripheral neuropathy.

    A 32-year-old man sought medical advice because of impotence. He had been married for 8 years and had two children aged 6 and 4 years. Previous sexual activity had been satisfactory. Two months before seeking advice he had developed total failure of erection and ejaculation, but claimed that sexual desire was undiminished. On direct questioning it was learnt that there were no morning erections and he had experienced frequency of micturition for 6 months and urgency for 2 months. On two or three occasions during the previous 6 months he had noticed a tendency to constipation. There was no past medical history, or family history of a similar complaint.

    He was a healthy male with no abnormality on general examination including the genitalia. Neurological examination revealed normal tone and power in all four limbs but the tendon stretch reflexes were brisk. There were three beats of clonus at each ankle; the plantar responses were flexor.

    Questions

    1. What anatomical structures are involved?

    2. What investigations are indicated?

    3. What is the prognosis for improvement?

    4. What treatment can be given?

    Answers

    1. Impotence commonly is of psychological origin. The combination of impotence with bladder and bowel dysfunction suggests an organic neurological cause. Anatomically, this may be attributable to a lesion in the parasympathetic nerve supply to the bladder, bowel and sexual organs, or secondary either to spinal cord or cauda equina disease or to an autonomic or generalized peripheral neuropathy. Certain drugs, e.g. methyldopa and β-blockers, can also cause impotence alone.

    2. The neurological signs are non-localizing and not always of pathological significance. They exclude a peripheral neuropathy and, although it is unlikely that there will be structural disease involving the spinal canal, this should be excluded by myelography and the CSF examined for cells, protein and immunoglobulin content.

    3. Impotence due to organic neurological disease has a poor prognosis and if it persists for more than a few months is likely to be permanent.

    4. Mild sedatives and androgens have been used in treatment. A penile implant may assist in maintaining erections. There are encouraging reports of the use of implanted cauda equina nerve stimulators in producing both erections and ejaculation in impotent men. Ejaculation can also be achieved by electrostimulation of the prostate.

    Comment

    Myelography was normal; there was a CSF pleocytosis with increased IgG, suggesting a diagnosis of demyelinating disease – a not infrequent cause of this combination of symptoms in young men.

    Further reading

    APPENZELLER, O., ‘The reflex control of copulatory behaviour and neurogenic disorders of sexual function’The Autonomic Nervous System. Amsterdam: Elsevier Biomedical, 1982. [Chapter 16].

    Case 1.2

    An evolving paraparesis

    Publisher Summary

    This chapter reviews a medical case of an evolving paraparesis. A 48-year-old woman presented with a short history of difficulty in walking and a tendency to trip over on the left leg. She had been unwell for 3 months during which time she had fallen twice, catching her toes on a kerbstone. There was no pain, but gradually, her walking deteriorated and her friends noticed that she was unsteady. She had developed mild urgency and frequency of micturition. Two months previously, she had, for the first time, experienced tingling in the fingers of the left hand. She had seen her general practitioner at the age of 21 because of an episode of pain and visual impairment in the left eye, lasting 8 weeks; she had been told that this was because of neuritis. There was no other past medical or family history. The combination of an evolving paraparesis and history of an episode of visual loss thought to be because of optic neuritis is highly suggestive of demyelinating disease. The ataxia may be attributable to cerebellar lesions but could also be because of disease in the cerebellar connections of the spinal cord.

    A 48-year-old woman presented with a short history of difficulty in walking and a tendency to trip over on the left leg. She had been unwell for 3 months during which time she had fallen twice, catching her toes on a kerbstone. There was no pain, but gradually her walking deteriorated and her friends noticed that she was unsteady. She had developed mild urgency and frequency of micturition. Two months previously she had, for the first time, experienced tingling in the fingers of the left hand.

    She had seen her general practitioner at the age of 21 because of an episode of pain and visual impairment in the left eye, lasting 8 weeks; she had been told this was due to neuritis. There was no other past medical or family history.

    General examination was normal. In the cranial nerves the only abnormality was left optic disc pallor. The upper limbs were normal. She had increased tone in the legs with a pyramidal distribution weakness on the left. Tendon stretch reflexes were brisk and there was sustained clonus at the left ankle. There was no sensory abnormality. She was mildly ataxic in both legs and on tandem walking. Examination of the spine was unremarkable.

    Questions

    1. These statements concerning this patient may be true or false:

    (a) Paraplegia following RBN is compatible with multiple sclerosis.

    (b) Her ataxia may be explained by a lesion in the spinal cord.

    (c) Delayed VEP and SSEP latencies would suggest multiple sclerosis.

    (d) Investigation should include examination of the CSF.

    (e) Treatment with steroids might be expected to reduce the severity of the symptoms.

    Answers

    1. 

    Enjoying the preview?
    Page 1 of 1