Cranial Nerves 2025 PDF by Hamada Zehry

Cranial nerves Dr / HAMADA ZEHRY, MD Lecturer of Neurology , Horus University Cranial Nerves 12 pairs of cranial nerves, marked with Roman numerals I-XII for identification. All originate from nuclei in the brain. Functions could be sensory or motor o...

Cranial nerves Dr / HAMADA ZEHRY, MD Lecturer of Neurology , Horus University Cranial Nerves 12 pairs of cranial nerves, marked with Roman numerals I-XII for identification. All originate from nuclei in the brain. Functions could be sensory or motor or mixed.  Case Scenario : A 23-year-old male presented with one month history of loss of smell preceded by severe head injury one and half month back. Systemic and neurological examinations were non-contributory except loss of olfaction on both sides. Causes of Anosmia: Nasal (odorants do not reach the olfactory mucosa): Examples—viral infection of upper respiratory tract, allergic rhinitis, nasal polyps, THE and heavy smoking. Olfactory neuroepthithelial damage (due to destruction of receptors or their axon OLFACTORY filaments as they pass through cribriform plate): Examples—head injury disrupts olfactory fibers prior to decussation. NERVE:- Central (due to olfactory pathway lesion): Examples— olfactory groove meningioma, giant aneurysm of anterior cerebral artery or anterior communicating artery, glioma of frontal lobe, and multiple sclerosis Olfaction in neurodegenerative diseases: Impaired olfaction may be one of the early or preclinical manifestations of a number of neurodegenerative disorders, e.g., Alzheimer’s disease, idiopathic Parkinson’s disease, and Lewy body disease. Age-related decline in smell function Causes of Parosmia Sinusitis, depression, and temporal lobe epilepsy. Causes of Olfactory Hallucination Temporal lobe epilepsy (uncinate seizures), alcohol withdrawal, and depression.  Foster–Kennedy Syndrome Components: THE Ipsilateral anosmia due to direct pressure over olfactory bulb or tract OLFACTORY Ipsilateral optic atrophy due to direct pressure over the optic nerve on the same side. NERVE:- Contralateral papilledema due to the mass lesion leading to increased intracranial tension. Example: Olfactory groove meningioma may cause Foster– Kennedy syndrome.  Case Scenario : A 21-year-old woman reported progressive diminution of vision in her right eye for last 8 days. One day prior to the onset of visual impairment, she had pain over her right THE OPTIC forehead that worsened during eye movements. On examination, visual function was normal in the left eye. In NERVE right eye, visual acuity was 6/60 with no improvement with pinhole and there was no color perception along with relative afferent pupillary defect. Visual field examination showed a central scotoma. The fundi were normal. Extraocular movements and the rest of systemic and neurological examination were normal. THE OPTIC NERVE Examination of IInd Cranial Nerve Visual acuity Color vision Field of vision Fundus (fundoscopy) Primary optic atrophy: The disc is flat and quite white with clear cut edges. It is due to local lesions of the optic nerve such as, ischemic neuropathy, pressure on the nerve, optic neuritis, injuries, toxins e.g. tobacco, alcohol, lead, …etc; tabes dorsalis and certain familial disorders e.g. leber's disease. Optic atrophy Secondary (consecutive) optic atrophy: The disc is grayish-white in color and its margins are indistinct (blurred). It follows swelling of the optic disc due to papilledema. Temporal pallor: The disc is apparently pale in quadrantic or crescentric manner on the temporal half due to lesion principally of the papillomacular bundle. This is often seen in cases of multiple sclerosis, but it is neither constant in that disease, nor pathognomonic of it.  Optic nerve swellings This is of two types: A- Papilledema: This is swelling of the optic nerve head due to increased intracranial pressure. Fundoscopic appearance varies according to the stage of the papilledema. The followings are the different stages of evolution of papilledema: THE OPTIC 1. Engorgement of the retinal vessels. 2. Blurring of the disc margins. NERVE 3. A redder disc with loss of the physiological cupping of the disc. 4. Advanced stage: In addition to the above findings, there are a lot of retinal hemorrhages and exudates. B- Papillitis: This is due to a local disease that affects the optic nerve head. There is hyperemia and some swelling of the optic disc. It must not be confused with papilledema in spite of their ophthalmoscopic appearances. Oculomotor nerve (CN III), Trochlear nerve (IV) and Abducens nerve (VI)  The third, the fourth, & the sixth cranial nerves (The oculomotor, the trochlear, & the abducent nerves) Extraocular muscles are (4 recti,2 oblique and The levator palpebrae superioris originates) All extraocular muscles , 7 in Extra ocular number , supplied by 3rd cranial nerve except lateral rectus by 6th nerves cranial nerve and sup. Oblique by trochlear nerve Examination of the ocular nerves is aimed to look for and analyse the following ocular signs: 1) Ptosis. 2) Proptosis. 3) Pupils (anisocoria) 4) Squint. 5) Diplopia. 6) Nystagmus. Action of extra ocular muscles Lesions of extra ocular nerves Ptosis means drooping of the eyelids reaching the pupil and covering part of it. Proptosis It is forward displacement of the eyeballs. It is best detected by examination of the patient in profile or from above. Miosis An abnormally small pupil (miosis) is a sign of lesion in the sympathetic pathway which supplies the pupillary dilator muscle. Mydriasis (dilated pupil) a variety of lesions, some of them purely ocular, such as uveitis, may give rise to a fixed dilated pupil. Neurologically, there are three main diagnostic considerations: 1)Surgical Third nerve palsy. 2)Non-reactive pupils. 3)Light-near dissociation. Third nerve palsy it is characterized by the following (4 Ds) features: Drooping of eyelids (ptosis). Divergent squint. Diplopia. Dilated pupil.  Oculomotor nerve (CN III) PALSY  A lesion of CN III can affect all or only a portion of the nerve (i.e., complete or partial CN III palsy).  A complete CN III palsy would thus be expected to produce - Ipsilateral dilated pupil ( paralysis of sphincter pupillae muscle ) (internal ophthalmoplegia). - Ptosis. (levator palpebrae superioris muscle weakness) - External ophthalmoplegia involving all of the extraocular muscles innervated by CN III (i.e., superior rectus, inferior rectus, inferior oblique and medial rectus muscles).  The most common causes of acquired third nerve palsy : - Microvascular occlusion (DM, HTN,…). - Trauma - Compression from neoplasm or Sixth nerve palsy it is characterized by the following features: 1) Convergent squint (in turning of the eye)—failure of abduction of the eye. 2) Diplopia in the primary position and on looking toward the direction of the paretic muscle. 3) Compensatory head tilt towards the side of the lesion. Fourth nerve palsy it is characterized by the following features: 1) The affected eye tends to deviate upward and inward. 2) Vertical diplopia: The patient complains of difficulty in reading and ongoing downstairs. 3) Extortion and weakness of downward movement of the affected eye when the eye turned inward. 4) Head tilting to the opposite shoulder to obtain single vision when looking forward. Diplopia  Double vision, also called diplopia, causes an individual to see two overlapping sets of images. Binocular diplopia refers to double vision due to misalignment of the eyes, often caused by weakness or restricted movement of the muscles surrounding the eye (i.e., extraocular muscles).  Binocular diplopia occurs when both eyes are open, so it can resolve when one eye is covered or closed.  There are many potential causes of binocular diplopia, including problems with the eye muscles (PM), neuromuscular diseases (MG), damage to the cranial nerves (III, IV, and VI), systemic diseases ( Graves’ disease )and neurological or brainstem (stroke and MS) disorders. The etiology and presentation of acquired third-nerve lesions at various levels are different:  Trigeminal nerve palsy (CN V): The trigeminal nerve is the largest of the cranial nerves. It provides sensory input from the face and motor innervation to the muscles of mastication (masseter and pterygoids muscles).  Causes of trigeminal nerve palsy include: - central causes due to a lesion in the pons, medulla and upper cervical cord: o Tumors / syringobulbia /vascular - peripheral causes include: o Tumors / aneurysm /chronic meningitis - a lesion of the trigeminal ganglion: o acoustic neuroma / meningioma /fracture of the middle fossa - a lesion in the cavernous sinus: Tumors / aneurysm / thrombosis The latter is associated with III, IV and VI palsies Trigeminal neuralgia Trigeminal neuralgia (TN) is characterised by recurrent, unilateral, brief (