User:Neurokostar

Symptoms of Nervous System �   — are divided into four classes★ Deficit symptoms Irritative symptoms Liberated symptoms Shock Symptoms Disorders of consciousness ---   �Clinical classification Disturbances of the level of consciousness ★ Somnolent Stupor coma Aphasia---Concept Aphasia★ Disorders of communication with others in language caused by lesions in cerebral. Disorders of repetition, naming, reading and writing. Though the patient has normal consciousness, mental status and voicing structures, but he loses his ability of reading, speaking, hearing and writing (dictation). Broca Aphasia ---Clinical features The patient knows what he or she wants to say but has difficult in finding the correct words, often product the wrong word. The ability to repeat words is better than spontaneous speech. Broca Aphasia --- Lesions The lesion locates in the motor speech area the posterior of inferior frontal gyrus of dominant hemisphere.

Wernicke Aphasia---Clinical features The speech is fluent but is replaced with partly incorrect word ( paraphasia) or newly created meaningless words (neologisms). Thus the speech does not make sense but the patient has poor insight into the problem. Wernicke Aphasia --- Lesions The lesion locate in the sensory speech area. It lays in the posterior part of superior temporal gyrus of the dominant hemisphere Anomic Aphasia---Clinical features the patient can’t name the objects that  he is familiar with. But he know how to use them and whether you name them  correctly or wrongly.

The lesion locates in anomic speech area. The posterior part of media temporal gyrus or the borderline between temporal lobe and occipital lobe  of the dominant hemisphere. Bilateral hemianopia loss of the temporal side of visual field in both eyes. Caused by the optic chiasm lesion such as pituitary tumor、craniopharyngioma.

Oculomotor nerve palsy ptosis outward deviation diplopia disorder of Eye Movement : upward. downward. inward dilatation of pupil, abolition of light reflex loss of reaction to accommodation

Pupillary and reflexes�                 --- Clinical features Pupillary abnormalities★ Anatomy and Physiology Pupils size: In a brightly illuminated examining room, the normal diameter of pupils in adults are 2~4mm Less than 2mm --- constriction of pupil． More than 5mm --- dilatation of pupil．

Pupillary light reflex Pathway: retina→optic nerves→optic chiasma→optic tract→pretectal area→ Edinger-Westphal nucleus→oculomotor nerves→ciliary ganglion→postgangliar fibers→pupillary constrictor muscles Eye Movement Disorders�               --- Clinical features Reaction to accommodation When the eyes focus on a nearer object, the pupils normally constrict. Argyll-Robertson pupil pupillary light reflex(-), accommodation reflex(+), neurosyphilis is the usual cause. Adie pupil (tonic pupil) Unilateral larger pupil, constrict slow to persistent bright light

Horner sign clinical features: unilateral lesion. small pupil (myosis) ptosis enophthalmus lack of sweating in the face. Lesions： damage of cervicum upper sympathetic nerve or fibra of sympathetic nerve in reticular formation of brainstem

Irritative Symptoms Hypersthesia ★ It refers to the perception of a light stimulus as an abnormally great sensation. Hyperpathia ★ The period of sensation  is longer than in a normal person. The condition is often accompanied with mood changes, thalamic pain and so on.

Irritative Symptoms Dysesthesia ★ The feeling to stimulus are not uniform. e.g while touch is given, the patient feels pain. Paresthesia ★ Subjective sensations No objective stimulus, the patient  have feelings of  numbness, formication,  expanding, cold, warmth, tingling, pressure, etc.) Dissociated anesthesia Some sensating are affected while others are intact. Usually  pain and temperature senses are lost but sense of touch , position and vibration are intact. This occurs in syringomyelia

Brown sequard Also called Spinal cord hemisection syndrome deep sensory disorder and spastic paralysis on the same side below the level of lesion pain and temperature loss of the opposite side below the level of lesion.

Tri-partial syndrome Hemianesthesia, hemiplegia and hemianopia of the opposite side

Hemiparesis 3 hemi signs Contralateral hemiparalysis (central facial nerve palsy and hypoglossal nerve palsy) Contralateral hemihypoesthesia Contralateral homonymous hemianopia

Cerebellar Ataxia The cerebellum and its connections are responsible for the coordination of skilled voluntary movement, posture and gait.

Cerebellar dysfunction causes impairment of the process of initiating, stopping, and controlling movements.

1. Cerebellar ataxia --- Clinical features (1) Disorders of posture and gait Ataxia gait: a wide base with staggering gait. In mild cases, the unsteadiness may be apparent only walking heel-to-toe (tandem walking) In a unilateral cerebellar hemisphere lesion, there is unsteadiness towards the side of the lesion. In cerebellar tonsil lesion--- truncal ataxia, there is difficulty sitting or standing without support and the patient tends to fall backwards. 1. Cerebellar ataxia - Clinical features (2) Incoordination of movement Intention tremor: coarse oscilating Dysdiadochokinesia: inability to carry out rapid alternating movements with regularity. Dysmetria: inability to carry out smooth and accurate targeted movements with overshooting of the target, as manifested by the finger-nose and heel-knee-shin tests.

3. Cerebellar ataxia - Clinical features (3) Dysarthric speech Slow and slurred or scanning in quality Loss of variation of intonation The words may be broken up into syllables. 1. Cerebellar ataxia -Clinical features (4) Abnormal eye movements Jerky pursuits: pursuit movements are slow, with catch-up saccadic movements on attempt to maintain lixation on the moving target. Dysmetria of saccades: on attempt to fixate on a target, the eyes overshoot and oscillate several times before fixation is achieved. Nystagmus: this is maximal on deviation of the eyes towards the side of the lesion. It is results from damage of the vestibular connections of the cerebellar. 1.Cerebellar ataxia -Clinical features (5) Hypotonia A relatively minor feature of cerebellar diseases Decreased resistance to passive movements ‘Pendular’ tendon reflexs The rebound phenomenon With the patient’s arms outstretched, his forearms are pressed down and then abruptly released by the examiner, the arm may rebound upwards much further than usual in the presence of cerebellar hypotonia. LP Indications It is indicated for the following purpose： 1. Diagnosis for some diseases meningitis and other infective or inflammatory disorder subarachnoid hemorrhage hepatic encephalopathy meningeal malignancies paraneoplastic disorders suspected abnormalities of intracranial pressure

�Indications � 2. Assessment of the response to therapy ( in meningitis and other infective or inflammatory disorders). 3. Administration of intrathecal medications or radiologic contrast media. 4. Rarely to reduce cerebrospinal fluid (CFS) pressure.

LP Contraindications 1. Suspected intracranial mass lesion. (To avoid hasten incipient transtentorial herniation) 2. Local infection overlying the site of puncture. 3. Coagulopathy. (Clotting-factor deficiencies or rapidly failing platelet counts should be corrected to reduce the risk of hemorrhage) Contraindications 4. Suspected spinal cord mass lesion. ( only in association with myelography,        which is used to determine the presence         and level of structural spinal pathology) Parkinsons Also called paralysis agitans. A common degeneration disease in     nervous system. It becomes increasingly common with advancing age. It is characterized by rest tremor, rigidity, bradykinesia, abnormal gait and posture.

Pathology loss of pigment cells in the substantia nigra and locus coeruleus and dorsal vagal nucleus and other pigment cell  degeneration and necrosis Cell loss in the globus pallidus and putamen The presence of filamentous eosinophilic intraneural granules (Lewy body),  containing the protein alpha-synuclein ,in the basal ganglia ,brainstem ,spinal cord ,and symptomatic ganglia Loss of DA neurons in SNpc and DA neurons degenerate

Clinical  findings★ Over middle aged Insidious onset Gradual progression, “N” progression Four cardinal signs

Clinical  findings 4.Four Cardinal Signs- Trap Tremor Rigidity Akinesia and bradykinesia Posture and gait abnormalities Gait Disorder Loss of Balance

Over middle aged, Insidious onset, Gradual progression Akinesian and bradykinesia At least one of the three cardinal signs Tremor Rigidity Postural and Gait Disorders Response effectively to levodopa No other neurologic positive signs Segments of spinal cord and spine The spinal cord of C1~8 is one segment higher than the correspond spine respectively, T1~8 is two segments higher, T9~12 is three segments higher, lumbar cord lies in the level of the 10~12th  thoracic vertebra , sacral cord lies in the level of the 12th thoracic vertebra and the 1st lumbar vertebra.

Acute myelitis Acute myelitis is an acute inflammation of one or more segments of the spinal cord, which is associated with infections and vaccinations disorders. Acute transverse impairments caused by demyelination or necrosis of the myelin on white matter. Clinical findings Acute transverse myelitis Onset Age range :   --the youth & post adolescent ,4 to 83 years; Mean 32 to 44 years gender:    male ≈female --no difference Initial Symptoms: --- Numbness and weakness ---Backache and girdle sensation on the segment of lesion. Episode: --- Acute onset, getting to the peak after several hours to 3 days. Progression < 4 weeks Diagnosis Acute onset The history of infection and vaccination. The symptoms and signs of transverse impairment weakness, sensory disorders, autonomic nerve dysfunction The examinations of CSF and MRI

1.History of herpes labialis or genital herpes ； 2.Acute onset, prodromal symptoms of fever and general malaise; 3.features of psychiatric symptom, consciousness disorder , seizure and focal neurological system sign 4.CSF: the increasing of WBC and RBC, glucose and chloridum is normal 5.EEG shows diffuse slow-wave, mainly in temporal and frontal lobes. 6.Head CT or MRI shows focal hemorrhagic necrotizing lesion in temporal lobe. 7.antiviral treatment is effective.

It often follows 1-4 weeks after a respiratory infection, inoculations or surgical procedures or diarrhea. Campylobacter jejuni(CJ) has been particularly implicated as a cause of the diarrhea. Clinical features GBS First symptoms Weakness: Most often symptomatic in legs Pain: Low back & legs Paresthesias: Distal-- Subjective cutaneous sensations (cold, warmth, tingling, pressure, etc.) that are experienced spontaneously in the absence of stimulation. GBS CSF CSF: - a characteristic abnormality. --- CSF Albumino-cytological dissociation ---increased concentration of protein but a normal cell count in the 2rd and 3th week. Test of CSF is normal in the first week. Protein Early (1st 2 days): Usually (85%) normal Later High; 66% in 1st week; 82% in 2nd week Cells: Normal (~90%), unless associated disorder present

Trigeminal neuralgia Trigeminal neuralgia we discuss is primary ( or idiopathic) trigeminal neuralgia. Trigeminal neuralgia is a facial-pain syndrome  of unknown  cause that develops in middle to late life, and  is an acute transient, recurrent attack  of agonia in the sensory distributions of  the 5th cranial  nerve.

Trigeminal neuralgia Clinical features 1. It develops in middle to late life. female > male. mainly adults, especially the elderly. 2.The clinical characters of the pain 3. special findings 4. Course  is  repeated. 5. Neurological examination is normal. There is no loss of taste, hearing, or sensation in someone suffering from tic douloureux. Bell’s palsy Hunt syndrome ---lesions : above geniculate ganglion 1. Hyperacusis (hypersensitivity to sound in the affected ear ) 2. Dysgeusia (loss of taste on the front two-thirds of the tongue ) 3. Lower motor neuron facial palsy 4. Pain of Near mastoid process at the  effected face. 5. Loss of pinna and auditory canal’s sensation. 6. Herpes of periost