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Approach to patients with isolated cranial nerve lesion:-
A patient coming with disorder of sense of smell. The leading cause of olfactory disorders are Viral infections Bacterial Rhinitis, allergic Rhinitis, deviated nasal septum, polyps, and some times trauma to head. Viral infections destroy the olfactory neuroepithelium. Cranial trauma is followed by uni- or bilateral impairment of sense of smell in 5 to 10% of cases. some times there may be associated CSF rhinorrhea
In an old patient, consider the possibilities of Presbyopia, Cataract, Glaucoma or Macular degeneration. Vision can be impaired by damage to the visual system any where from the eyes to the occipital lobe. One can localise the site of lesion with considerable accuracy by mapping the visual field defect by finger confrontation and then correlating it with the topographic anatomy of the visual pathway. A patient presenting with scotoma confined to one eye must be due to a lesion anterior to the chiasma involving either optic nerve or retina. At the optic chaisma, fibers from the nasal ganglion cells decussate in to the contralateral optic tract. Crossed fibers are damaged more by the compression than the uncrossed fibers. As a result lesions of the sellar region causes a temporal hemianopia in each eye. In a patient who is able to read only the left or right half of the eye (Snellen's) chart consider unilateral post chiasmal lesions, which may leave the visual acuity in each eye unaffected. Occlusion of the posterior cerebral artery supplying the occipital lobe is a frequent cause of total homonymous hemianopia. Some patients with hemianopia, after occipital stroke have macular sparing because the macular representation at the tip of occipital lobe is supplied by collaterals from the middle cerebral artery. Destruction of both occipital lobes produces cortical blindness. This condition can be distinguished from bilateral prechiasmal visual loss by noting that the pupil responses remain normal. Patients describing a rapid fading of vision like a curtain descends some times affecting only a portion of the visual field, consider Transient Ischaemic attack of the retina (Amaurosis fugax). It usually occurs from an embolus that become stuck with in a retinal arterioles. In hypertensive crisis, sudden visual loss can result from vasospasm of retinal arterioles and consequent retinal ischaemia. Optic neuritis is a common inflammatory disease of the optic nerve. Most of the patients experience a gradual recovery of vision after a single episode of optic neuritis. Internal carotid artery occlusion lead to hemiplegia and central retinal artery occlusion.
Approach to a patient presenting with double vision The first point to clarify is whether diplopia persists in either eye after covering the fellow eye. If it does, the diagnosis is monocular diplopia. The cause is usually intrinsic to the eye. Diplopia alleviated by covering one eye is binocular diplopia and is caused by disruption of ocular alignment. Enquiry should be made in to the nature of the double vision, mode of onset, duration, intermittency, diurnal variation and associated neurologic or systemic symptoms Myasthenia gravis is a major cause of diplopia. The diplopia is often intermittent variable and not confined to any single ocular motor nerve distribution. The pupils are always normal. Fluctuating ptosis may be present. A patient presenting with ptosis, dilated pupil and eye looking down and out, consider oculomotor nerve lesion because of the unopposed action of the Lateral Rectus and Superior Oblique. This combination of finds are obvious. Any combination of ptosis, pupil dilation and weakness of the eye muscles supplied by Oculomotor nerve may be encountered. The advent of Oculomotor nerve palsy with any degree of pupil involvement in an otherwise healthy patient, especially when accompanied by pain raises the suspicion of Circle of Willis aneurysm. Lesion of oculomotor nucleus in the rostral mid brain produces bilateral ptosis because the Levator muscle is innervated by a single central subnucleus. Third nerve is affected in Disseminated Sclerosis and Cavernous sinus thrombosis. Nothnagels syndrome:- Injury to the superior cerebellar peduncle causes ipsilateral Oculomotor palsy and contralateral cerebellar ataxia. Webers syndrome:- Injury to the cerebral peduncle causes ipsilateral oculomotor palsy with contralateral hemiparesis. (Crossed hemiplegia) In a patient complaining of vertical diplopia especially on reading or looking down, consider Trochlear nerve palsy. The vertical diplopia is exacerbated by tilting the head towards the side with palsy and alleviated by tilting it away. This head tilt test is a cardinal diagnostic feature. {The principal action of this muscle (Superior oblique) is to depress and to intort the globe} The patient climbs down the stairs with compensatory neck turn to opposite side A patient presenting with horizontal diplopia when looking to one side consider Abducent nerve palsy. Fovilles syndrome:- Dorsal pontine injury resulting in lateral gaze palsy, ipsilateral facial palsy, and contralateral hemiparesis. Unilateral or bilateral Abducent nerve palsy is a classic sign of raised intra cranial pressure. The mechanism is probably due to rostral -caudal displacement of brain stem. A patient presenting with deafness, pain and ipsilateral Abducent palsy, it can be Gradenigos syndrome due to affection of petrous apex in mastoiditis. The frontal eye field of the cerebral cortex is involved in the generation of saccades to the contralateral side. After hemispheric stroke, the eyes usually deviate towards the lesioned side because of unopposed action of the frontal eye field in the normal hemisphere. Seizures generally have the opposite effect, the eye does deviate conjugately away from the irritative focus. Neurons in the paramedian pontine reticular formation are responsible for controlling conjugate gaze towards the same side. A lesion of either the paramedian pontine reticular formation, or the Abducens nucleus causes an ipsilateral conjugate gaze palsy. A lesion of the medial longitudinal fasciculus that interrupts the impulse from the center for lateral gaze in the lower pons to the third nerve nucleus in the mid brain causes a dissociation of the conjugate eye movements. This is called Inter nuclear ophthalmoplegia. Prese3nce of inter nuclear ophthalmoplegia indicates usually an intrinsic brain stem lesion like multiple sclerosis or infarct of brain stem Abnormal pupil reflexes:- Argyll Robertson pupil - Light reflexes is abolished and accommodation reflex is present (Neuro syphilis) Home-Adie pupil (Tonic pupillary reaction)- The light reflex appears to be absent or it may be present but delayed. Once the pupil constricts it may persist. Horners Syndrome- Miosis, ptosis, enophthalmos, blood shot conjunctiva and anhydrosis of ipsilateral half of face (due to damage of sympathetic pathway) Hutchison's pupil- Pupil constricts initially, later dilates in one side, by the time other pupil constricts then again dilates (in extra dural hematoma, extensive intracranial bleeding, extensive infarct with gross cerebral oedema.)
A patient presenting with sensory impairment over the face, Horner's syndrome and ataxia on one side and impaired pain and temperature sensation on the other side- It can be Lateral medullary syndrome (Wallenbergs syndrome) Due to occlusion of branches of vertebral artery A patient presenting with dysarthria, palatal muscle, tongue and pharyngeal muscles are spastic, and on examination jaw jerk is exaggerated. It is due to pseudobulbar palsy.
A patient presenting with deviation of angle of mouth, absence of nasolabial fold, fore head unfurrowed, eye lids which do not close and epiphora, then it may be due to Lower motor neuron type of facial paralysis and site of lesion at the stylomastoid foramen. Commonest cause is Bells palsy. Other causes are parotid tumour, Leprosy, Gillen-Barry syndrome. A patient complaining of loss of taste of anterior 2/3rd of tongue on the same side of facial palsy and also hyperacusis. The lesion is distal to Geniculate ganglion and in addition to above symptoms loss of lacrimation and salivation lesion may be at the internal auditory canal. Causes are Bells palsy, Mastoiditis, Herpes zoster (Ramsay-Hunt syndrome). Patient presenting with unilateral LMN type of facial palsy and also complaining of deafness and tinnitus causes may be acoustic neuroma or meningioma of cerebral pontine angle. A patient presenting with ipsilateral facial weakness and diplopia when looking towards the side of facial weakness and also have also contralateral hemiparesis the lesion occured at the nuclear level. Common causes are infarction, haemorrhage, tumour, demyelinating disease of pons. Patient presented with loss of voluntary contraction of lower part of facial muscles but preserved mimetic movements. This is an volitional type of facial palsy and occurs in lesions of corticonuclear fibers of facial nucleus. When patients presents with loss of involuntary movements during crying, smiling but voluntary movements are preserved. This is mimetic type of UMN type facial palsy, occurs in lesions in the basal ganglia, thalamus, hypothalamus on prefrontal lobe. Patient presenting with mask like facies with loss of both volitional and mimetic movements. This can be mixed type of UMN paralysis occurring in Parkinsonism. Patient presenting with UMN type of facial paralysis and hemiparesis on the same side- lesion is at the cortical level on the opposite side. Causes include infarction, haemorrhage, tumour, multiple sclerosis.
Patient at the age of 50 have recurrent vertigo accompanied by tinnitus and deafness- Meniers disease. Patient complains of paroxysmal vertigo and nystagmus with certain positions of the head - Benign positional vertigo Vertigo of less severe and loss frequently paroxysmal may be an vestibular nerve origin and cause acoustic neuroma.
Cochlear nerve must be tested in detail in patients who talk loudly. Patient complaining of sudden onset of unilateral hearing loss with or with out tinnitus - cause can be viral infection of the middle ear. Patient complains of gradual progression in hearing defect cause include otosclerosis, noise induced hearing loss, acoustic neuroma, Meneres disease.
Patient with intense throat pain in the region of tonsilar fossa and pain initiated by swallowing and radiation to the ear- the condition is Glossopharyngeal neuralgia
Patient complaining of dysphagia, dysphonia on examination soft palate droops ipsilaterally and does not rise on phonation, voice is hoarse and vocal cords lies immobile in cadaveric position - Vagal nerve palsy [ in diphtheria pharyngeal branches of both vagus may be affected then voice has a nasal quality and also regurgitation of fluids] In bulbar palsy there is 9, 10, 11 nerves affection. the symptoms of the patient will be dysphagia, dysphonia and nasal regurgitation. Causes are Lateral medullary syndrome, motor neuron disease, (thyroid superior lobe tumour) Gag reflex and palatal reflux will be absent in this case.
Patient comes with torticollis and drooping of shoulders resulting from partial or complete paralysis of accessory nerve
Patient presenting with dysarthria and difficulty in chewing and swallowing. On examination there is wasting of muscles of tongue and fasciculations It ay be a Bulbar type of paralysis of 12th nerve. If the tongue is spastic it can be pseudobulbar palsy In Medullary syndrome there is paralysis of the ipsilateral half of the tongue with contralateral hemiparesis. The face is spared. In addition there is impaired proprioceptive sensations contralaterally. |
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