The dysfunction of certain cranial nerves can affect the eye, the pupil, the optic nerve or the eye muscles and their nerves; thus they can be considered disorders of the cranial nerves, neuro-ophthalmologic disorders or both. Neuro-ophthalmologic disorders can also include a dysfunction of the central tracks for control and integration of eye movements and vision. Disturbances of the cranial nerves and the dysfunction of smell, sight, chewing, facial sensory and expression, taste, hearing, balance, swallowing, phonation, turning the head and lifting the shoulder or tongue movements can include (see Table: cranial nerves). It can be affected one or more cranial nerves.

(Horner’s syndrome, dementia: symptoms and complaints, the visual pathway and the visual pathway). The dysfunction of certain cranial nerves can affect the eye, the pupil, the optic nerve or the eye muscles and their nerves; thus they can be considered disorders of the cranial nerves, neuro-ophthalmologic disorders or both. Neuro-ophthalmologic disorders can also include a dysfunction of the central tracks for control and integration of eye movements and vision. Disturbances of the cranial nerves and the dysfunction of smell, sight, chewing, facial sensory and expression, taste, hearing, balance, swallowing, phonation, turning the head and lifting the shoulder or tongue movements can include (see Table: cranial nerves). It can be affected one or more cranial nerves. Cranial nerves. Cranial nerve nerve function Possible findings Possible causes * olfactory nerve (I) Provides sensory input of smell anosmia head trauma disorders of the nose (eg., Allergic rhinitis) Neurodegenerative diseases (eg., Alzheimer’s dementia, Parkinson’s disease) Sinusitis tumors fossa, nasal cavity and paranasal sinuses, optic nerve (II) Provides sensory input for seeing Amaurosis fugax (transient monocular blindness), unilateral loss of the top or bottom field of embolic the ophthalmic artery ipsilateral internal carotid disease embolism of the retinal arteries anterior ischemic optic neuropathy (also called “disk at risk”) “Crowded papilla morphology” complications after cataract extraction connective tissue disease that causes (eg arteritis. B. temporal arteritis, anti-phospholipid antibody syndrome), diabetes mellitus hypotension or, if hard hypovolemia Ipsilateral blockade of the internal carotid artery phosphodiesterase type 5 (PDE5) inhibitors (eg. As sildenafil, tadalafil, vardenafil) of embolism retinal arteries optic neuritis (papillitis and retrobulbar) Acute demyelinating diseases (eg. as multiple sclerosis, neuromyelitis optica) Bacterial infections (eg. as tuberculosis, syphilis, Lyme disease) post Infectious viral infections (eg., HIV, herpes simplex, cytomegalovirus) toxic-nutritional optic neuropathy (toxic amblyopia) drugs (chloramphenicol, ethambutol, isoniazid, streptomycin, sulfonamides, digitalis , Chlorpropamide, ergot alkaloids, Disulfiram) methanol uptake malnutrition, if hard Organic mercury compounds Vitamin B12 deficiency Bitemporal hemianopia craniopharyngioma meningioma of tubercle sellae saccular aneurysm in the cavernous sinus suprasellar extension of a pituitary adenoma oculomotor nerve (III) Cancels the eyelids moving the eyes above, below posterior and medial adjusts the light in the eyes of focusing lenses paralysis aneurysm communicating artery ischemia III. Cranial nerve (often by disease of small vessels as in diabetes mellitus) or its fascicles in the midbrain transtentorial entrapment by intracranial mass (z. B. subdural hematoma, tumor, abscess) trochlear nerve (IV) moving the eye inwardly and downwardly over the obliquus superior paralysis often idiopathic head trauma infarction often by disease of small vessels (eg. as in diabetes mellitus) tentorial-meningioma pinealoma myokymia the superior oblique (usually with short episodic eye movements that cause subjective visual shimmer, nystagmus, and / or sc hiefe view) entrapment of the trochlear nerve (through a vascular loop similar trigeminal (V) Augenast as in the pathophysiology of trigeminal neuralgia) N. (N. ophthalmicus) Returns sensory input from the eye surface, the lacrimal gland, scalp, forehead, upper eyelid neuralgia compression of the nerve root by vascular loop multiple sclerosis (occasionally) lesions of the cavernous sinus or the superior orbital fissure upper and ramus (maxillary nerve and N. mandubularis) Returns sensory input of teeth, gums, lips, gums and mucosa facial skin lesions neuralgia of the cavernous sinus (maxillary nerve), multiple sclerosis (occasionally) compression of the nerve root by vascular loop Moves the muscles of mastication (chewing, teeth grinding) neuropathy carcinomatous or lymphomatous meningitis connective tissue meningiomas, schwannomas or metastatic tumors of the skull base abducens (VI) moves the eye to the outside (abduction) via the lateral rectus palsy often idiopathic head trauma Increased intracranial pressure tissue diseases (with CNS involvement z. B. neurosarcoidosis) infections or tumors which affect the meninges multiple sclerosis nasopharyngeal carcinoma Pons- or cerebellar tumors pontine infarction Wernicke encephalopathy facial nerve (VII) Move the facial muscles Proximal branches: innervate the lacrimal and salivary glands and provide sensory input for taste the anterior two-thirds of the tongue paralysis vestibular schwannoma Schädelbasisbruch idiopathic facial paralysis (Bell’s Palsy), Guillain-Barre syndrome infarctions and tumors of the pons Lyme disease Melkersson-Rosenthal syndrome Ramsay Hunt syndrome sarcoidosis tumors that invade the temporal bone relapsing uveoparotidea (Heerfordt syndrome) Hemifacial spasm compression of the nerve root by arterial vascular loop vestibulocochlear (VIII) Returns sensory input for balance and hearing tinnitus, dizziness, feeling of pressure in the ear and hearing loss M. Meniere barotrauma Benign paroxysmal positional vertigo age-associated Otolithenaggregation in the rear or horizontal canal, in connection with age and / trauma or infection (occasionally) vestibular neuritis viral infections Hearing loss or hearing acoustic neuroma aging barotrauma cerebellopontine angle tumors Congenital rubella infection exposure to loud noise hereditary diseases meningitis viral infections (possibly) glossopharyngeal (IX) Returns sensory input of the throat, tonsils, posterior tongue and carotid arteries glossopharyngeal compression of the nerve by ectasia artery or tumor (rare) Moves the muscles for swallowing and salivary gland to blood pressure regulation involved Glossopharyngeusneuropathie tumor or aneurysm in the posterior cranial fossa or jugular foramen vagus nerve (X) moving vocal cords and the muscles for swallowing transmits pulses to the heart, and smooth muscles of viscera hoarseness, dysphonia and dysphagia vasovagal syncope entrapment of the recurrent laryngeal nerve through mediastinal herpes zoster Infectious or cancerous meningitis Medullary tumors or ischemia (eg. B. lateral medullary syndrome) accessory nerve (XI) rotary head Controls shrugging Partial or complete paralysis of the sternocleidomastoid muscle and trapezius Iatrogenic (eg., By lymph node biopsy in the rear neck triangle) Idiopathic trauma tumors of the skull base or in close to the meninges hypoglossal (XII), the tongue atrophy and fasciculation of the tongue Intramedullary lesions motion (z. B. tumors) lesions of the basal meninges or occipital bone (z. B. Platybasie, Paget’s disease of the skull base) surgical trauma (e.g. ., by Endar teriektomie) motor neuron disease (e.g.. As amyotrophic lateral sclerosis) * Diseases that cause diffuse motor paralysis, (z. B. myasthenia gravis, botulism, variant of Guillain-Barre syndrome, poliomyelitis with bulbar involvement) often affect the cranial nerves. Amyotrophic lateral sclerosis can cause significant fasciculations of the tongue. Causes and Symptoms neuroophthalmologischer disorders and diseases of the cranial nerves overlap. Both types of noise may be due to tumors, inflammation, trauma, systemic Erankungen and degenerative or other processes that cause symptoms such as loss of vision, double vision, ptosis, pupillary abnormalities, periocular, facial and headache. Diagnosis The evaluation includes: Detailed questions on the symptoms review of the visual system tests to detect a nystagmus (nystagmus) investigation of the cranial nerves The review of the visual system includes an ophthalmoscope and testing of visual acuity, visual field (see table: investigation of eye diseases: perimetry ), pupils (see table: Common abnormalities of the pupils) and eye movements (Augenmotilität- see table: Common disorders of ocular motility). In this study, II., III., IV., And VI. Cranial nerve studied (Like the cranial nerves are to be assessed). Most also have a cranial imaging with CT or MRI is required. The following components of the visual inspection are of particular interest in the diagnosis of neuroophthalmologischen disorders and diseases of the cranial nerves. The pupils are inspected for size, equality and regularity. Normally, the pupils constrict prompt (within 1 s) and evenly during accommodation and in direct exposure to light as well as light that is directed to the other pupil (consensual light reflex). If a defect is present, can be determined using a back and forth swinging torch by testing the pupillary reaction to light consensual. Normally, the degree of pupillary constriction does not change when the flashlight swings from one eye to the other. In case of a relative afferent defect (deafferentierte pupil, afferent pupillary defect or Marcus-Gunn pupil), the pupil dilates paradoxically, when the flashlight to the side of the defect oscillates. A deafferentierte pupil narrows in response to consensual, but not direct light. When an efferent defect, the pupil responds sluggishly or not at both direct and on consensual light. Common abnormalities of the pupils finding Declaration asymmetry of 1-2 mm between the pupils, reactions to light received and no symptoms Normal variation (physiologic Anisocoria) asymmetry, impaired light reactions and received Akkommodationsreaktion (light-near dissociation or Argyll Robertson pupil) neurosyphilis (possibly) Bilateral narrowing opioids Miotic eye drops (in glaucoma most common; require unilateral constriction when only one eye is dropped) Pontine hemorrhage organophosphates or cholinergic toxins Double-sided extension (with preserved reflections Hyperadrenerge states z. B. withdrawal symptoms, drug / drugs such as sympathomimetics or cocaine, thyrotoxicosis) Double-sided extension with reduced direct light reaction Mydriatic eye drops such as sympathomimetics (z. B. phenylephrine) and cycloplegics (eg. B. cyclopentolate, tropicamide homatropine, atropine) herniation of the brain hypoxic or ischemic encephalopathy sided extension with afferent pupillary defect lesions of the eye, the retina or II. cranial nerve (optic nerve) Unilateral extension with efferent pupillary defect paralysis of III. Cranial nerve (oculomotor), often due to compression (eg. As by aneurysms of the posterior communicating artery, or by transtentorial herniation) Iris trauma (also irregular pupil) Mydriatic eye drops * sided extension with minimal or slower direct and consensual light response and pupillary constriction in response to accommodation tonic pupil (Adie pupil) † * transtentorial entrapment and use of mydriatic eye drops often can be distinguished in the dilated pupil by instillation of a drop of pilocarpine eye solution; takes place in response to any restriction, this speaks for mydriatic eye drops. † There is permanently a tonic pupil, but ciliary no progressive abnormal dilation of the pupil by damage to the ganglion. It occurs usually in women aged 20-40 years. The onset is usually sudden. The only findings are slightly blurred vision, impaired dark adaptation and sometimes lack of deep tendon reflexes. Eye movements are checked by the patient holds his head still while he pursues the finger of the examiner, as this is (from far right to left, top to bottom, moving diagonally to either side and nose of the patient to the accommodation to judge). In such a study, however, a discrete paresis of eye movement can be overlooked, which, however, sufficient to cause diplopia. EineDiplopie may have a defect of the reversible coordination of the eye movement (for. Example, the neural pathways) or III. (Oculomotor), IV. (Trochlear) or VI. (Abducens) show cranial nerves. If the diplopia remains, while one eye is closed (monocular diplopia), the cause is presumably in a non-euro logical eye disease. Disappears diplopia when one eye is closed (binocular diplopia), the cause is probably a disorder of ocular motility. The two images are furthest away from each other when the patient looks in the direction which covers the paretic eye muscle (z. B. left if the left lateral rectus muscle is paretic). The eye which eliminates the further peripheral image in the closed state, is paretic. The paretic eye can be more easily identified if a red glass is held over one eye. When the red glass covers the paretic eye on peripheral image is red. Common disorders of ocular motility Clinical Findings syndrome Common causes paralysis of horizontal gaze palsy in a direction Conjugated horizontal palsy lesion in the ipsilateral pontine center palsy for horizontal viewing movements or in the contralateral frontal cortex horizontal in both directions Total (on both sides) horizontal palsy Wernicke encephalopathy Extensive bilateral pontine lesion which affects both centers for horizontal viewing movements bilateral paralysis of all horizontal eye movement other than the abduction of the eye contralateral to the lesion; the convergence is not affected one and a half syndrome lesion in the medial longitudinal fasciculus and in the ipsilateral pontine center for horizontal eye movements Unilateral or bilateral paresis of Augenadduktion for horizontal lateral eye movements, but not in convergence. Internuclear ophthalmoplegia lesion in the medial longitudinal fasciculus Vertical gaze palsy (usually at Aufblick) with dilated pupils, often in combination with a convergence paralysis, failure of the pupillary reflex, response to light worse than on convergence, downward view preference and nystagmus with a fast impact direction component downward. (Editor’s note: The Parinaud syndrome is not uniformly defined, here a common definition is given.) Parinaud syndrome (a type of conjugated vertical gaze palsy) Pinealistumor Dorsal means cerebral infarction both sides paresis of the conjugate after downward eye movements paresis of Abblicks progressive supranuclear palsy unilateral eye deviation (the rest position is located below and outside); unilateral paresis of Augenadduktion, raising and lowering, ptosis, often dilated pupil paralysis of III. (Cranial nerve aneurysms ischemia in oculomotor nerve or middle cerebral trauma transtentorial entrapment Unilateral paresis of the downwardly and inwardly (nasal) directed eye movement, which can be hardly recognizable and symptoms (difficulty to look downwardly and inwardly) leads hyperextension mark of the head of patient tends head to the side opposite to the affected eye) paralysis of the VI. Cranial nerves Idiopathic head trauma ischemia Congenital Unilateral paresis of Augenabduktion paralysis of the VI. Cranial nerves Idiopathic infarction vasculitis Increased intracranial pressure Wernicke encephalopathy multiple sclerosis oblique deviation (vertical misalignment of the eyes) and unequal Partial participation of the nuclei of the III. Cranial nerves, the Center for vertical eye movements or the medial longitudinal fasciculus brainstem lesion External anywhere between midbrain and medulla weakness or limitation all extraocular muscles Ophthalmoplegia dysfunction of the eye muscles or the neuromuscular junction Usually due to the following causes: myasthenia gravis Graves’ disease botulism Mitochondrial myopathies (eg . B. Kearns-Sayre syndrome) oculopharyngeal dystrophy Myotonic muscular dystrophy Orbital pseudotumor Involuntary or abnormal movements Rhythmic involuntary movements, usually bilateral nystagmus nystagmus. Faster downward jerk and slow return upwards to the middle position swings of the eyes ( “ocular bobbing”) Extensive pontine destruction or dysfunction Excessive eye movement, followed by several oscillations Augendysmetrie disorders Kleinbhirnbahnen accumulation faster horizontal oscillations about a fixed point eyes flutter Numerous causes: postanoxic encephalopathy occult neuroblastoma paraneoplastic effects ataxia telangiectasia-Viral encephalitis Toxic Effects of drugs / medicines Fast, conjugated multidirectional, chaotic movements, often in conjunction with myoclonus opsoclonus Numerous causes (like eyes flutter, s. above) Treatment Treatment neuroophthalmologischer disorders and diseases of the cranial nerves depends on the cause.

Health Life Media Team

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