Foot drop

A lesion of L5 causes weakness of ankle dorsiflexion, inversion and eversion and dorsiflexion of the great toe. A lesion of S1 causes weakness of plantar flexion, eversion and knee flexion, and an absent ankle jerk. Therefore a foot drop in association with the loss of the ankle jerk will only occur with involvement of both L5 and S1.

Spinal cord compression

In spinal cord compression, local or radicular pain is the most frequent and earliest clinical symptom. Clinical examination in the early stages can be unremarkable. However, subsequent weakness and bladder and bowel dysfunction can develop.

The diagnosis of spinal cord compression must always be considered even if the clinical examination is normal. The diagnosis can be confirmed by MRI, which is considered superior to CT imaging or myelography. Lumbar puncture should be avoided as herniation of the cord into a decompressed region can result following the removal of cerebrospinal fluid. Manometry and cytological analysis are unlikely to give diagnostic information and may worsen the situation due to the lumbar puncture.

Patients with rapidly progressive neurological signs should be considered for neurosurgical decompression, and radiotherapy is useful in the treatment of slowly progressive lesions. Systemic chemotherapy and corticosteroids should not be used in place of surgery or radiotherapy, and may not influence the clinical situation.

Effect of Antiepileptic Drugs on Oral Contraceptives

Metabolism of the OCP and the POP is accelerated by:

• Carbamazepine
• Phenytoin
• Phenobarbitone
• Oxcarbazepine
• Topiramate. 

The higher oestrogen (50mcg) containing OCP preparations are more effective than the typical lower dose preparations (30mcg) in patients on enzyme inducing medication, but are still approximately 10 times less effective than in women on the 30mcg preparations who do not take anti-epileptic medication.

There is no evidence that the metabolism of Depo-provera is affected by anti-epileptic medication.

Delirium

A sudden change in the mental state or sudden onset of behaviour that is out of character in an older person is most likely to be due to an acute confusional state (delirium). Even if a patient is confused it is paramount to take a history, which may give clues to the cause of the delirium. It also gives you the opportunity to assess the severity of confusion. The patient will benefit from reassurance. Of course, don’t dismiss the possibility that the patient is not confused and her jewellery is indeed missing! A physical review and review of investigations must be done as soon as is possible as delirium is a serious condition with a high morbidity and mortality. Sedation should only be used as a last resort and preferably only once the cause of the delirium has been established.

Vestibulocochlear Nerve (Cranial Nerve VIII)

From the auditory nuclei in the brain stem impulses are transmitted to the inferior colliculus and medial geniculate body of both sides through the trapezoid body and the lateral lemnisci. From there they reach the auditory cortex via the auditory radiations.

Inferior colliculus – lateral lemniscus - medial geniculate body

From the cerebellopontine angle the vestibulocochlear nerve enters the internal acoustic meatus along with the facial nerve (the trigeminal nerve does not pass through the cerebellopontine angle). In the inner ear it innervates the maculae of the utricle and saccule as well as the cristae of the semicircular ducts.

The vestibular ganglion is associated with the vestibular nerve whereas the spiral ganglion is a part of the cochlear nerve which innervates the organ of Corti.

The auditory pathway from the inner ear to the auditory cortex is via the lateral lemniscus, inferior colliculus, medial geniculate body and auditory radiation.

Subacute combined degeneration of the cord

Subacute combined degeneration of the cord is caused by vitamin B12 deficiency. The early signs usually include loss of vibration sense and position sense. There is usually a symmetrical peripheral neuropathy, which is associated with absence of ankle reflexes. The sensory ataxia leads to a positive Rhomberg's sign. Knee reflexes are often brisk and plantars are extensor due to pyramidal involvement causing upper motor signs.

Vitamin B12 deficiency may also cause optic atrophy and confusion.

Paraneoplastic conditions

Paraneoplastic conditions can occur up to several years before the emergence of the underlying tumour. The pathophysiological basis is thought to be autoimmune. A wide variety of clinical syndromes have been described affecting central structures, such as the mesial temporal lobes or spinal cord, or peripheral elements including nerve and muscle.

Dermatomes

L2,3 radiates to the anterior thigh.

L5 radiates through the buttock, down the posteriolateral aspect of the thigh, lateral aspect of calf and across the dorsum of the foot to the big toe.

S1 radiates through the inner buttock to the posterior aspect of the thigh, posteriolateral aspect of the calf to the lateral border of the foot.

Diagnosis of Subarachnoid Haemorrhage (SAH)

Fig 1: Subarachnoid Haemorrhage

CT brain scan is normal in up to 30% of patients with SAH, so that a negative scan cannot be used to exclude the diagnosis if suspected clinically. However, a positive CT brain scan enables the diagnosis to be made non-invasivally.

Fig 2: CT and MRI brain show Subarachnoid Haemorrhage (SAH)

Absence of red blood cells, or the absence of xanthochromia is sensitive for the exclusion of SAH. Where lumbar puncture (LP) is traumatic, the presence of large numbers of red cells may complicate interpretation. In this situation, spectophotometric analysis of the supernatant for red cell pigments may be helpful. 

Bilirubin and oxyhaemoglobin take 12 hours to appear in the cerebrospinal fluid (CSF) following a bleed, and for this reason LP should usually be delayed until more than 12 hours from the onset of symptoms. 

Because of the invasive nature of cerebral angiography, and relatively high complication rate, it is usually reserved for patients whose other investigations are positive.

Fig 3:
a) CT showing subarachnoid haemorrhage,
b) Cerebral angiograms demonstrating 13 aneurysms,
b)3 in the right anterior circulation
c) 5 in the left anterior circulation, and
d) 5 in the posterior circulation.
Arrow heads, aneurysms;
arrow, ruptured aneurysm

Source: Fig 1, Fig 2, Fig 3, 

Subarachnoid Haemorrhage

The investigation of choice in suspected subarachnoid haemorrhage (SAH) is immediate CT scan without contrast, taking very thin cuts through the base of the brain to optimise the chances of seeing small collections of blood. Imaging within 12 hours using modern scanners has a 98-100% sensitivity for SAH.

Lumbar puncture should be performed in suspected SAH if the CT scan is not diagnostic. The CSF specimen should be centrifuged without delay and examined by spectrophotometry for the presence of xanthochromia due to the presence of oxyhaemoglobin and bilirubin. Note, however, that xanthochromia may not be present if the CSF is examined within 12 hours of haemorrhage occurring, so lumbar puncture should be delayed for 24 hours.

Tuberculosis Meningitis

The combination of space-occupying lesions, high CSF protein, low CSF glucose and CSF lymphocytosis point to this case being tuberculosis meningitis with cerebral tuberculomas. The organism is not seen on microscopy in 20-50% of cases. Cryptococcal meningitis can give a similar picture, although the protein and glucose changes are not usually so marked; cerebral cryptococcomas are uncommon and the organism is normally seen on microscopy in patients as ill as this. Toxoplasmosis, syphilis and lymphoma would not cause such significant changes in the protein, glucose or white cell count.

Schwannomas

These relatively rare benign tumours are nonetheless the most common tumour of the peripheral nerves, and may affect any nerve in the body. They arise from the sheath surrounding the nerve (Schwann cells). In Schwannomas, cells are not organized like Schwann cells around the axons but instead in swirls and streaks across and among themselves. Schwannomas do not invade the nerve and can usually be surgically removed without damage to the adjacent nerve.
Schwannomas usually grow very slowly but they can become very large. Very large tumours can be seen or felt as a bulge under the skin.
Schwannomas (like neurofibromas) can occur singly or multiply. Multiple Schwannomas can occur on many different nerves or be limited to only one nerve or to one extremity.
Schwannomas (and neurofibromas) are seen in association with Neurofibromatosis (‘von Recklinghausen’s disease’). Schwannomas and neurofibromas look very similar on MR.
Although Schwannomas are benign (they do not metastasise), a small number (5-15% quoted in the literature) are more aggressive and some can even become malignant (malignant transformation) and very rarely metastasise. Watching with serial imaging and clinical examination is a reasonable approach but surgery may be best if there is any increase in size or more aggressive appearance. Schwannomas can often be removed with little injury to the nerve that they grow on, as opposed to neurofibromas whose removal usually requires division of the nerve around the tumour.

Optic Disc

The optic disc lies nasal (medial) to the macula lutea. It is normally circular or oval in shape, becoming more oval if astigmatism is present. It is paler than the rest of the retina.

The physiological cup is a central depression in the disc, whereas the fovea centralis is a depression in the centre of the macula.

The physiological cup is deeper in glaucoma.

Diabetic Eye Disease

Foveal oedema

Fig 1: The fovea: this is the view of an eye a doctor sees looking,  just like a map. The central area of the retina is the 'macula', shown by the dotted black ring. Light focuses here, so any damage may affect a sight. The very central area, the yellow dot, is the the fovea.

Distortion and micropsia arise when the photoreceptors within the deeper layers of the retina become irregularly spaced. Such symptoms are typical of diabetic maculopathy, but not typical of proliferative retinopathy which is characteristically asymptomatic until an acute vitreous haemorrhage occurs.

Cataract occurs at an earlier age than usual in diabetes, but these symptoms are not typical.

Retinal vein occlusion may also present with foveal oedema but is less likely as a cause, especially in a relatively young woman without extra vascular risk factors.

Oral hypoglycaemic medication does not cause foveal damage. Although transient blurring of vision may occur when the blood sugar is first brought under control, this is more typical of type 1 diabetes, in which normalization is more rapid and more profound after using insulin for the first time.

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The appearances are of background diabetic retinopathy with hard exudates in a circular or circinate pattern at the fovea. Blot haemorrhages are also seen, but there are no new vessels to indicate diabetic proliferative retinopathy. The fact that the fovea is involved in this case will mean that the patient’s vision is affected and the eye can be described as showing ‘maculopathy’.

Diabetic maculopathy as seen here will be treated by focal or ‘grid’ laser coagulation, the primary goal being to seal leaking areas close to the fovea.

Wernicke’s encephalopathy

Wernicke’s encephalopathy typically presents with ophthalmoplegia (horizontal and vertical nystagmus, weakness / paralysis of the lateral rectus muscles, weakness / paralysis of conjugate gaze), ataxia (predominantly affecting stance or gait, and often without clear-cut intention tremor) and confusion.

Horizontal nystagmus

Vertical nystagmus

Lateral rectus muscle

Conjugate gaze