Common abnormalities

• With unilateral atrophy the tongue becomes wrinkled and thinner on the affected side and deviates towards that side on protrusion.

• Spontaneous contraction (fasciculation) of small parts of the muscles may be apparent and more easily seen when the tongue is protruded.

• Unilateral XII nerve lesions are usually seen with other cranial neuropathies, and the eatiscs may be neoplastic (skull base tumour), vascular (medullary infarct, vertebral artery aneurysm) or traumatic.

• Bilateral lower motor neurone lesions may be seen as part of a wider clinical syndrome (e.g. motor neurone disease or syringobulbia) and are often components of bulbar palsy.

• Myopathic disorders involving the tongue will generally be part of a more widespread syndrome (e.g. myasthenia gravis). Such lesions cause dysarthria, dysphagia and dysphonia.

• Unilateral upper motor neurone lesions may produce deviation of the protruded tongue which is not associated with fasciculation or wasting. This is most typically seen immediately after an acute cerebrovascular event; the asymmetry of tongue protrusion tends to resolve after several days.

• With bilateral upper motor neurone lesions, voluntary movements of the tongue are hypokinetic (slow) and the tongue appears small and tends to assume a more conical form. There tends to be dysarthria and dysphagia. Such dysfunction (pseudobulbar palsy) may occur in


• The commonest cause of anosmia is obstruction of the nasal passages.

• The field lor red colour vision is much smaller than that lor monochrome.

• tl a lesion occurs dislal to the optic chiasma, the same side of each visual field will be affected In each eye and the defect is termed homonymous.

• The superior oblique muscle Is supplied by the IV cranial nerve and is responsible for downward movement of the adducted eye.

• Conjugate ocular motility is dependent not only on the integrity of the cranial nerves but also on a central brain stem tract, the medial longitudinal fasciculation (MLF).

• Parasympathetic fibres constrict and sympathetic fibres dilate the pupil.

• In many cases a VI cranial nerve palsy is a 'false localising' sign caused by raised intracranial pressure.

• Minor degrees of nystagmus are seen in normal patients a( extremes of lateral gaze, particularly if maintained for more than 10 seconds.

• Pendular nystagmus is often due to long-standing poor visloa

« Unilateral loss of sensation in one or more branches of the trigeminal nerve is an important finding.

« A pathologically brisk jaw jerk occurs in patients with bilateral upper motor neurone lesions above the level of the pons.

m An upper motor neurone lesion affecting one corticobulbar (facial) tract results in relative sparing of the upper lace because of bilateral innervation of those muscles.

• In clinical practice deafness is olten best studied using audiometry.

• Many patients with vertigo and tinnitus have no detectable abnormality on clinical examination.

• IX cranial nerve dysfunction is usually seen with other signs of cranial nerve or brain stem dysfunction.

• With lesions of the recurrent laryngeal branch of the vagus nerve, the voice will sound hoarse and the cough bovine.

• Inspect the trapezius muscle from behind.

• Orofacial dyskinesias are usually drug Induced.

supranuclear or suprabulbar disorders, which may he vascular (e.g. bilaleral insular infarction) or inflammatory (e.g. multiple sclerosis) in origin.

• Orofacial dyspraxias involve inability so move the tongue and parts of the face on command and are usually seen after parietal lobe lesions.

• Involuntary movements of the tongue (and usually parts of the facial musculature as well) may occur in a group of disorders called orofacial dyskinesias. These are most often drug induced (e.g. major tranquillisers, antiparkinsonian drugs) and may persist, or even worsen, after drug withdrawal. They may he choreiform in type or tremulous in some patients.

• Lesions of the cranial nerves IX. X. XI and Xll may be simultaneously affected, usually by diffuse disorders -typically motor neurone disease. The condition is known as bulbar palsy with clinical features of dysphonia. dysarthria and dysphagia.

Where there are bilateral supranuclear lesions of IX—XII due to vascular disease, motor neurone disease or demyelinalion, there is loss of voluniary palatal and pharyngeal movements. but with an intact gag reflex (pseudobulbar palsy).

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Essentials of Human Physiology

Essentials of Human Physiology

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