central nervous system-theory

8/8/2019 Central Nervous System-Theory

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CENTRAL NERVOUS SYSTEM-theory

COMA:

The reticular activating system extends from upper brain

stem-pons, mid-brain and thalamus.There is a connection

to the cerebral cortex, but for the level of

consciousness,the degree of wakefulness is related to the

mass of functioning cortex which is affected.The degree of

decrease in alertness depends on the acuteness of onset.

Herniation

- Tentorial which affects III rd cranial nerve

-Herniation of cerebellar tonsils through the foramen

magnum

Causes-

Hypoxia,hypoglycemia,ischemia,hyponatremia,hyperosm

olarity,

Hypercapnia,hepatic failure,renal failure,hyperthermia,

hypothermia,Drugs-Barbiturate,Morphine and alcohol.

Infection- Encephalitis, Meningitis,Gram negative

septicemia.

Hemorrhage- into basal ganglia, thalamus,pontine,

cerebellar.

Basilar artery thrombosis.


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Head injury.

History - Drugs,Alcohol,Trauma,cardiac arrest,preceding

neurologic symptoms,history of liver,kidney or lung

disease.

Exam

- TPR BP

- Effects of alcoholism

- Evidence of internal hemorrhage

- MI

- GN Septicemia.

- Addisons disease.

- Fundus exam useful in sub-arachnoid

hemorrhage,hypertensive encephalopathy and other

causes of increased intra-cranial tension.

- CNS- 1)The nature of respiration and the

spontaneous movements are observed without

disturbing the patient.

2) Decorticate rigidity- flexion and supination of upper

limb and extension of lower limb.

3) Decerebrate rigidity- evidence of mid-brain damage-

extension of upper and lower limbs.

4) Focal neurologic deficit.

5)Elicited movements and level of arousal.


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6) Brain stem reflexes-Pupils and conjugate eye

movement.

Investigations- CT

- MRI

- CSF

- Blood serum electrolytes,Blood sugar,Blood urea

nitrogen,Liver function tests.

Emergency treatment-

1) Correct BP, Blood sugar level,O2,CO2, Hypo/ hyper-

thermia

immediately.

2) Airway.

3)I.V Access- Glucose,vitamin B1.

PARKINSONISM

Incidence -Common in middle/late life, gradually

progressive and prolonged course. 1-2 per 1000, I per 100

in patient > 65 yrs M=F.

Mechanism- Dopamine and acetyl choline imbalance in

the basal ganglia,they modulate the thalamus which is

normally inhibited by GABA.


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Causes -

1) Post- encephalitic.

2) Arteriosclerosis.

3) Trauma- punch-drunk

4) Drugs- Reserpine

5) Toxins- manganese,cobalt,copper ( Wilsons disease).

6) Shy-Drager syndrome

7) Creutzfeldt-Jakob disease.

Pathology -

Nerve cell loss with reactive gliosis in substantia nigra,

intra-cytoplasmic inclusion bodies- Lewy bodies are

found.Decreased dopamine levels are present in caudate

nucleus and putamen.

Clinical Features -

1) Tremors- rhythmic,flexion-extension of fingers,

hand or foot on one or both sides pill rolling

tremors.

2) Rigidity.

3) Akinesia

4) Fixity of facial expression- wide palpebral fissures

- infrequent blinking

- blepharospasm, blepharoclonus.


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5) Voice low, no modulation, monotonous.Speech

slurred.

6) Gait- short shuffling steps, festinant gait, person

seems to be running after his own center of

gravity.

7) Posture-flexion of the limbs and trunk.

8) Glabellar tap- no adaptation.

9) In later stages- mental depression and dementia.

Differential diagnosis-

- Depression.

- Benign essential tremors.

- Normal pressure hydro-cephalus.

- Huntingtons disease.

Treatment-

- Selegiline 5 mg b.i.d.

- L-DOPA ( 100/250 mg) + carbidopa (25mg )

- Bromocriptine 15-30 mg/day.

- Pergolide 2-6 mg/day.

- Tri-hexi-phenidyl 2 mg t.i.d.

- Amantidine 100 mg b.i.d.


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CEREBRO-VASCULAR DISEASE-

The brain weight is 2% of the body weight but receives

17% of the cardiac output.If the blood supply to the brain

stops the patient will become unconscious within 10

seconds.

The internal carotid artery divides into anterior and

middle

cerebral arteries.

The vertebral arteries( branches of the subclavian) join

together to form the basilar artery which in turn divides

into 2 posterior cerebral arteries.

The Circle of Willis is formed by a connection between

the 2 anterior cerebral arteries in the form of the anterior

communicating artery,anteriorly and a connection

between the posterior cerebral artery and the middle

cerebral arteries.

Cerebral auto-regulation- is the mechanism by which the

blood supply to the brain is maintained inspite of wide

variation in the blood pressure.When the BP falls there is


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vaso-dilatation and when the BP rises there is vaso-

constriction of the cerebral vessels.

Internal Carotid branches- ophthalmic,hypophyseal, ant.

choroidal and post. communicating artery.

Middle cerebral artery- frontal, parietal, and temporal.

Anterior cerebral artery- supplies the corpus callosum, medial

part of the frontal and parietal lobes.There is also the

Recurrent artery of Heubner which supplies the internal

capsule (face and upper limb), caudate nucleus and putamen.

Vertebro-basilar system-

Vertebral artery- branches

-anterior and posterior spinal arteries.

-Posterior inferior cerebellar artery.

Basilar artery- branches

- anterior inferior cerebellar artery.

- Labyrinthine artery

- Pontine artery

- Superior cerebellar artery

- Posterior cerebral artery-with temporal,calcarine

and parieto-occipital branches.

Cerebro-vascular disease- includes diseases of cerebral vessels,

heart disease or blood dyscrasias.


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Cerebral Infarct- causes-

-Atherosclerosis

-Hypertension

-Congenital- aneurysms

-trauma ( to the neck)

-arteritis.

-infections

-malignancy.

Cerebral embolism

- atheroma of large vessels.

- Aneurysms of large arteries with mural thrombus.

- Cardiac-Infective endocarditis, Atrial fibrillation

with thrombo-embolism,MI, Cardiac surgery.

Risk factors- Hypertension,DM,Heart disease, Cigarette

smoking, dyslipidemia, increased hematocrit, alcohol, OC

pills,previous history of TIAs, cervical bruits.

TIAs

Carotid system -

-Contra-lateral hemiparesis.-Hemi-sensory loss.

-Hemi-anopia.

-Dysphasia.


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-Vision loss.

Vertebro-basilar system - vertigo, diplopia,blurred vision,

facial paresthesia/numbness, facial

weakness,dysarthria,dysphonia,ataxia.

Giddiness alone is not sufficient to diagnose as TIA.

Subclavian steal syndrome.

On exam- look for hypertension,peripheral vascular

disease,cardiac abnormalities.

Investigations-CBC,ESR,Blood urea,Serum

electrolytes,CXR,ECG.

In selected cases, CT scan,Echocardiography, and

angiography.

Treatment-

Control risk factors.

If cardiac source of embolism- anti-coagulants.

Surgery- Endarteterectomy.

Anti-platelet agents-Aspirin 150-300 mg/day.

CEREBRAL INFARCT-In the acute phase of illness, cerebral

edema ( maximum for 3-7 days.

In embolic strokes, the infarct can become hemorrhagic.


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Clinical features-It can present with an abrupt onset or with

slow worsening over hours to days ( stroke-in-evolution).The

clinical features depend on the site of block, presence of

collaterals.

Anterior cerebral artery involvement -

Corpus callosum,medial part of frontal and parietal lobes

affected.Recurent artery which supplies the part of internal

capsule controlling the face,upper limb and caudate nucleus

and putamen.

Presents as

-Contra-lateral hemiplegia ( shoulder and foot affected).

-Contra-lateral hemi-anesthesia.

-head and eye turned towards the lesion.

-Apraxia.( Ask the patient to perform simple tasks like

brushing teeth, using the pen)

-Akinetic mutism.

-Grasp and reaching reflex.

Middle cerebral artery involvement -

The motor area, sensory area, speech area, and auditory areas

affected.Presents as

- Hemiplegia,hemi-anesthesia.

- Homonymous hemi-anopia


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- Uninhibited bladder and bowel.

In the dominant hemisphere- global aphasia.

In the non-dominant hemisphere- affective agnosia,hemi-

inatention and visuo-spatial disorder.

Posterior cerebral artery involvement

- visual field defect,hemiparesis, sensory involvement.

- Patient may deny being blind- Antons syndrome.

- If angular gyrus involved (temporal and calcarine

branches) Gerstmanns syndrome-

- R-L dis-orientation,acalculia,dyslexia,agraphia,

finger agnosia.

Lacunar Infarct - multiple small deep,infarcts in the basal

ganglia,internal capsule and thalamus in hypertensive

patients.This can present as

-Pure motor

-Pure sensory

-Ataxic hemiparesis

-Clumsy hand-dysarthria syndrome.

Diffuse small vessel disease- presenting as dementia,

Parkinsonism, Pseudo-bulbar palsy and the presence of

primitive reflexes.

Multi-infarct dementia .

Medullary involvement - Lateral medullary syndrome


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-Lateral spino-thalamic tract- contra-lateral body loss of

pain, temp

-sympathetic fibres affected leading to Horners syndrome.

-Vagal nucleus- dysphagia,dysphonia.

-Vestibular nucleus- vertigo.

-Spinal nucleus of Trigenial nerve- ipsilateral face loss of

pain and temperature sensation.

-Spinocerebellar tract involved- unilateral cerebellar

involvement.

Pons - presnts with coma,quadriplegia,lateral gze

palsy,VII N., nystagmus,CVS/RS abnormalities,Jaw,

face, palate,tongue paralysis, locked-in syndrome

Midbrain

- III Nerve with hemi-paresis.

- III Nerve with cerebellar signs.

Investigations-

1. CT SCAN indications-

Young patient

Uncertain diagnosis of infarct

( D/D- hemorrhage, tumor,

cerebral abscess)

Inadequate history

Suspected hydrocephalus


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Sub-arachnoid/ intracerebral

hemorrhage suspected.

Continued deterioration after

stroke.

2.Angiography.

3.CSF ( Suspected sub-arachnoid hemorrhage)

4.Hematologic- Hb,TC,DC,ESR,Platelet count,Prothrombin

time,Partial thromboplastin time

5. Biochemical-RBS,Serum electrolytes, Renal function

tests,Liver function tests, Lipid profile.

6. ECG.

7. Chest X ray (aspiration)

8.Arterial blood gases ( adequacy of ventilation).

9. Anti-nuclear anti-body.

10.Assessment of the carotids, vertebral arteries and the heart.

Differential Diagnosis-

1) Chronic Sub-dural hematoma.

2) Herpes simplex encephalitis

3) Cerebral vein thrombosis.

4) Acute hypoglycemia.

Complications-

CVS/RS


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Neurogenic pulmonary edema

Cardiac arrhythmias

Pneumonia

DVT/Pulmonary embolism

Neuro-psychiatric -

Cerebral edema

Epilepsy

Spasticity

Contactures

Frozen shoulder.

Mental depression

Incontinence.

Renal/Metabolic -

UTI,Renal failure

Dehydration, electrolyte abnormalities.

SIADH

Hyperglycemia.

Miscellaneous Pressure sores,Weight loss/ gain

dependent edema.

Treatment- Though it is an emergency, stroke is not taken asseriously as an MI, therefore American Heart Association has

suggested the term brain attack and that a patient of stroke

needs to be closely monitored.


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30% of patients with stroke die of it.

Supportive

- prevent constipation using bulk laxative.

- Paracetamol for fever or pain.

- Bed rest (except for going to the toilet ) for 24 hours.

Anti-platelet agent/ anticoagulant, thrombolytic therapy (

risk of hemorrhage), hemorrheologic agents like

Pentoxifylline; oral nimodipine, Dexamethasone to reduce

cerebral edema.

Treat hypertension but not drastically.

Maintain nutrition and electrolyte balance- if unconscious

patient parenteral otherwise through Ryles tube. An

intake/output chart must be maintained.

Prevention of infection- UTI, aspiration pneumonia. Prevent thrombo-embolism- DVT by Heparin 5000

units SC 12 hrly; passive physiotherapy; compressive

stockings and early ambulation.

Prevent falls/ injury.

Surgical- endartectomy, embolectomy, and carotid

angioplasty.

Rehabilitation

Secondary prevention.


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Rehabilitation-

1) In patients with mild impairment- such as mild hemi-

paresis, hypesthesia, loss of balance- 1to 3 hour daily

individual and group OPD treatment.

2) If severe impairment- such as hemiplegia with spasticity,

visual- perceptual defects, complex aphasias,dysphagia,

other medical illnesses- 24 hour rehabilitation nursing

and > 3 hr. treatment in hospital.

3) Rehabilitation must match neurologic recovery, medical

stability, endurance and skill.

4) Early goals-

Self care, mobility, communication, cognition.

5) Rehabiliation is a team work including-

- Occupational therapist who focuses on daily living

activities and upper limb use.

- Physical therapist who focuses on mobility.

- Speech therapist who looks after communication,

swallowing and cognition.

- Others including rehalitation nurses, psychologists,

orthotists, recreational therpist and clergy.Prevention-

1.Anti-platelet drugs- prolonged use is beneficial. Aspirin 75mg

is effective.


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2. Treat hypertension.

3. Treat hypercholesterolemia if the patient is obese or has a

history of CAD.

4. Carotid endarterectomy in severe symptomatic carotid

artery stenosis.

5. Oral anti-coagulants are not effective and could be harmful.

6. In patients with AF and prior stroke or TIA- oral anti-

coagulants are used, if these are contra-indicated, aspirin can

be used.

CEREBRAL HEMORRHAGE-

Causes

- Hypertension.

- AV malformation.- Mycotic aneurysm

- Cortical thrombophlebitis.

- Hemangioma


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- Hemorrhagic telangiectasias.

- Hemorrhage into tumors.

- Hemorrhagic diseases- TCP,Hemophilia and sickle

cell disease.

Clinical Features-

6) Onset with headache, vomiting, generalized convulsions,

blurred

vision, dense hemiplegia and altered consciousness at the

outset itself.

7) Cerebellar hemorrhage- ataxia, headache, vomiting,

altered consciousness (brain stem hydrocephalus).

8) Pontine hemorrhage- loss of consciousness, fever, pin-

point pupils,brainstem reflexes lost- dolls eye manoeuvre

ve, conjugate gaze, extra-ocular movements,

quadriplegia.

Investigations-CT scan with contrast, Angiography.

Treatment Dexa-methasone , Surgery.


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VIRAL ENCEPHALITIS

Viruses-Echo, Coxsackie, Polio, Herpes Simplex virus,Rabies,

Yellow fever, Japanese B encephalitis,Mumps, Influenza,

Lymphocytic chorio-meningitis.

Pathology- Inflammation in the cortex, white matter, basal

ganglia, brainstem.Inclusion bodies in the cytoplasm and

infiltration with PMNs in the peri-vascular spaces.

Clinical features- acute onset headache, fever, vomiting,

altered consciousness drowsiness and coma, meningism (75

% cases), focal signs aphasia, hemiplegia, tetraplegia, cranial

nerve involvement ; generalized convulsions, features of raised

intra- cranial pressure.

In herpes simplex encephalitis- SOL like features, psychosis.

Investigations-

CBC

CT/MRI

CSF

- Clear

- proteins increased

- Sugar normal/ decreased- Increased lymphocytes

- Increased pressure

EEG

Serology/ Cell culture for identifying viruses.


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Differential Diagnosis-

1) Acute metabolic encephalopathy

2) Cerebral tumor

3) Stroke

4) Bacterial Meningitis/ cerebral abscess.5)Tuberculous meningitis.

Treatment- Fluid-electrolyte balance, Nutrition, Anti-

convulsants, Steroids, for Herpes simplex encephalitis-

Acyclovir 10mg/kg i.v. 8th hourly.

Brainstem Encephalitis- The patient complains of diplopia,

dysarthria,cranial nerve palsies.

NEURO-SYPHILIS

1. Meningo-vascular Syphilis - (5 years)

Endarteritis obliterans leading to stroke. Meningeal involvement- cranial nerve palsies.

Gumma- SOL like presentation / seizures.

2. Generalised Paresis of the Insane - ( 5-15 years )

Degeneration of the cortex presenting as

Dementia

Parkinsonian tremors.

Bil UMN signs

Delusion of grandeur.

3. Tabes dorsalis - ( 5-20 years )

Degeneration of sensory neurons,dorsal column wasting

and optic atrophy.


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Clinical features- lightning pain, sensory ataxia,

abdominal crisis, urinary incontinence, distal loss of deep

pain sensation- perforating painless deep ulcers,

Charcots joints, DTR diminished, hypotonia, Argyll-

robertsons pupil.

POLIO

Etiology and Epidemiology- The virus is a picorna virus with a

single stranded RNA and a capsid which binds to the cell

receptor.

The virus enters the GIT through the feco-oral route.GIT Sub-mucosal lymphatics, Peyers patches,Regional

lymph nodes.

? Peripheral nerves CNS.

? Viremia Muscles NM junction, motor nerves and

anterior horn cells.

Poor socio-economic status, poor hygiene.

Feco-oral infection

Patient is infectious before developing clinical features.

Incubation period 2-14 days.

90% infections are sub-clinical.

Clinical features-

1) Fever, sore throat, myalgia.


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2) 1% cases develop aseptic meningitis with severe neck

pain, back pain.

3) Paralytic type

- Severe muscle pain.

- Rapid/ slow onset muscle paralysis.- Proximal muscles affected, asymmetric involvement,

legs more commonly involved the arms, abdominal

and thoracic muscles may also be involved.

- Bulbar paralysis- presenting as dysphagia,

dysphonia, throat secretions.

- Respiratory failure maybe due to aspiration,

medullary center involvement or paralyis of phrenic

or intercostals nerves. 2/3 rds of these patients havea residual neurologic deficit.

Outcome in polio-

Varying degrees of muscle involvement in the limbs,trunk, pharynx, larynx and palate.

Maximum muscle weakness in 1 week.

Maximum recovery in 1 month.

If no recovery in 3-6 months then the prognosis is poor.

Risk to life if respiratory muscles or medulla involved.

Muscle involvement may lead to shortened contracted

limb with deformity. A small group of patients may show delayed deterioration

after many years.

Treatment-

Bed rest


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Assisted respiration

Prevent contractures by physio-therapy.

CARE OF PARAPLEGIC PATIENT

1. Prevent UTI Intermittent catheterization and

closed urinary system.

2. In acute paraplegia with spinal shock, CVS care as

paroxysmal sudden fluctuation of BP.

3. Ileus.

4. Stress ulcers- H2- blockers.

5. Risk of pulmonary embolism.6. Hypercalcemia due to immobilization.

7. In high cervical cord compression, respiratory

embarrassment and there is a need for endotracheal

intubation/tracheostomy. Sometimes ventilation and

suctioning if FVC < 12 ml/kg or PaO2 < 50 mm of

Hg.

8. Consider the psychologic state.

9. Nursing- Skin break down over pressure points.

- UTI

- ANS instability.

- Frequent repositioning, Skin emollients, soft bed

covering.

- Bowel regimens and dis-impaction.

10.Frequent severe hypertension, bradycardia may

occur in response to noxious stimuli in patients with

cervical or high thoracic cord compression. Thismaybe accompanied by flushing or sweating

11.Chest physiotherapy to prevent atelectasis or

pneumonia.

12. Splinting of limbs and passive exercises to prevent

contractures, foot drop etc.


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13.If patient has spasticity, painful flexor spasms or

adductor spasms,

- treat infections,skin ulcers, pain which act as

afferent impulses.

- Passive stretch- Oral/ intra-thecal Baclofen

- Inj. Botiulinum toxin into adductor muscles.

CEREBELLUM

It is required for muscle synergy and contraction of the

proper muscle at the appropriate time each with the

correct force. Anatomy - The cerebellum consists of the cortex ( grey

matter),the medullary center (white matter), 4 nuclei and

the superior, middle and inferior cerebellar peduncles,

which connect it to the mid-brain, pons and medulla

oblongata respectively.There are the flocculo-nodular

lobes and vermis and the cerebellar hemispheres.

Vermis ( midline zone)---------Intermediate zone-------Cerebellar

(Paravermis,

hemispheres

Stance Interposed nuclei)

Gait

Truncal ataxia

Ataxia of

limbs

Titubation of trunk

Dysarthria

Swaying and falling

Hypotonia

FNT

Nystagmus


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KHT Kinetic

tremors

Diseases of the cerebellum-

1. Hemorrhage

2. Cerebellar cortex degeneration alcoholic,

SA Degeneration sec. To gynec. tumors, oat

cell carcinoma, Hodgkins disease.Anti-

Purkinje cell antibodies are found.3. Encephalitis- involves the deep cerebellar

nuclei and presents with myoclonus.

4. Tumors of the cerebellum.

5. Demyelination.

SPINAL CORD

The spinal cord has 8 cervical,12 thoracic, 5 lumbar and 5sacral and 1 coccygeal segments, then it becomes the conus

medullaris and ends as the filum terminale. It has an anterior

and a posterior median sulcus.

It is covered by the meninges- the dura mater, the arachnoid

mater and the pia mater. It is anchored to the vertebra by the

ligamentum denticulatum. The parenchyma of the spinal cord

consists of gray matter and white matter, at the center of the

gray matter is the central canal which opens up into the and

terminates into the root of the filum terminale and containsCSF.

Gray matter- The amount of gray matter present in

the spinal cord corresponds to the amount of muscle tissue

supplied at that level.Therefore cervical and lumbar

enlargements have maximum amount of gray matter.


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Anterior gray column-

1) There are large multi-polar nerve cells, the axons of

which pass out as the -efferents to the skeletal muscles.

2) These are small multi-polar nerve cells whose axons also

travel in anterior roots as - efferents to the intra-fusalfibers of the muscle spindle.

The cells are divided into

Medial group-which supply the skeletal muscles of

the neck,trunk,intercostals and the abdominal

muscles.

Central group- Cervical-C4,5 & 6 which supplies the

diaphragm and at C5,6 some nerve cells innervate the

sterno-cleido-mastoid, the trapezius and theaccessory nucleus nerve fibers form the spinal part

of the accessory nerve.

Lateral group- in the cervical and lumbar

enlargements supply the skeletal muscles of the

limbs.

Posterior gray column-

1) Substantia gelatinosa- afferents from posterior root forpain and temperature also receive inputs from supra-

spinal levels.

2) Nucleus proprius-receives fibers related to the sense of

position, movement,2 point discrimination and

vibration.

3) Nucleus dorsalis-these cells are associated with neuro-

muscular spindles and tendon spindles.

4) Visceral afferents-from T1 to L3.

Lateral gray column-T1 to L2/3. give rise to pre-ganglionic para-

sympathetic fibers.

White matter-

Posterior column contains fibers which form the tracts of Gall

and Burdach which carry the sensations of fine touch,

vibration and joint position.


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Lateral column contains the lateral spinothalamic tract which

carries the sensations of pain and temperature, the anterior

and posterior spino-cerebellar tracts, the spino-tectal tract,the

spino-olivary tract,which are the ascending tracts;the

descending tracts are the rubro-spinal,the lateral cortico-spinaltract,the olivo-spinal and vestibulo-spinal tracts.

The anterior column- which contains the anterior or uncrossed

cortico-spinal tracts, and tecto-spinal tracts.

CORD COMPRESSION

The level of cord compression is most likely one at which there

is evidence of root involvement or LMN signs.

Symptoms- Root pain

Persistent flaccid paralysis

Wasting, fasciculations

Absence of DTR localizable to that segment.

Dermatologic evidence of sensory impairment with

normal sensation above that level.

Findings-1.If the level is between the cranio-vertebral junction to C5

quadriparesis.

2.If the level is between T2 and T12 paraplegia.

3.If the level is between C5 and T2 paraplegia with some

upper limb muscle paralysis.

If there is incomplete transection, the paresis.

If there is complete transection- then in the initial stage,

spinal shock follwed by paraplegia in extension thenparaplegia in flexion, then flexion contractures.

The spinal cord level below which there is weakness and

altered muscle tone is known as the motor level.

Loss of sensation occurs below the sensory level.

- gradation.


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- Zone of hyper-algesia above the sensory level.

Reflex level- above which reflexes are normal, below

which the reflexes are lost during the stage of spinal

shock and are increased in spastic paraplegia.

Disturbance of vaso-motor function,sweating occurs

below the level of the lesion due to disruption of the

central sympathetic fibers descending lateral columns.

Paralysis of bladder, rectal function and sexual

disturbance also occurs.

The level of the lesion will usually be at or above the

highest noted motor, sensory, reflex or autonomic level.

Brown-Sequard syndrome-

It occurs due to hemi-section of the cord. The features are Ipsilateral spastic paraparesis

Contra-lateral pain and temperature loss

Complete lesions are rare, but partial transection due

trauma or extra-medullary compression.

Conus medullaris- S3 or below involved.

Presents as saddle anesthesia, flaccid bladder, loss of anal

sphincteric control, absence of bulbo-cavernous reflexes and

anal reflex.Epi-conus- L4 to S2 involvement presents as lower limb

weakness- especially hip extension, flexion of knees and

movements of the foot and toes.

Cauda equina- results in compression of nerve roots L3 to S5.

Conus medullaris Cauda equina

1) Bilateral signs 1) Unilateral signs at theoutset.

2) Lower limb weakness not 2) Unilateral lower limb

weakness.

seen unless associated L3compression- quadriceps weakness


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and L3 hyper-algesia.

3) Saddle anesthesia 3) Root pain in the legs.

4) Early LMN bladder 4) Bladder involvement

rare, late.

5) Anal reflex absent 5) Anal reflex normal.

Extra- medullary Intra-medullary

Compression compression

1) Root pain, mid-line back 1) Dull ache in entire

limb,

pain increased by neck

flexion.

2) Brown- Sequard syndrome 2) Dissociated anesthesia.

3) Early CST signs 3) CST not prominent.

4) Early loss of sacral sensation 4) Sacral sensory loss

not seen.

5) CSF abnormal. 5) CSF normal.

Causes- arachnoiditis, neuro- Causes- astrocytoma,Fibroma, meningioma. Ependymoma.

Extra-dural compression-

Presents as low back pain worse on lying down, root pain.

Spinal tenderness, gibbus, kyphosis, para-vertebral muscle

spasm.

Causes-

1) Inter-vertebral disc prolapse- cervical or lumbar.

2) Metastases- from carcinomas or lymphoma.

3) Tuberculous Radiculo-myelopathy- there maybe

involvement of a single vertebra or adjacent vertebrae,

presenting as back pain, kyphosis, para-vertebral cold

abscess, slowly progressive para-paresis.


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4) Rheumatoid arthritis- causes atlanto-axial dis-location

leading to progressive tetra-paresis, dysarthria and

dysphagia due to compression of anterior spinal artery

and vertebral artery.

5) Tumors- presenting as back pain worse in lying position,root pain, local tenderness, progressive weakness and a

sensory level.

Investigations-

1) X-ray shows a lytic lesion.

2) MRI or CT scan.

3) Radio-nuclide scan.

4) Myelography.

Treatment- 1) Laminectomy2)High dose steroids

3) Fractionated radio-therapy.

NON-COMPRESSIVE MYELOPATHIES

1.Transverse myelitis

2.Vascular diseases- infarct, hemorrhage.3.Arachnoiditis.

4. Degenerative diseases- SACD, MND,Friedreichs

ataxia.

5. Toxic- SMON( due to hydroxy-quinolone),CO, As,

S, Lathyrism, Fluorosis, after spinal anesthesia.

6. Demyelinating disorders- multiple sclerosis.

7. Congenital anomalies- syringo-myelia.

8. Radiation myelopathy.

Transverse myelitis-

Post-viral- measles,mumps, herpes zoster.

Acute suppurative- a complication of pyogenic meningitis,

osteomyelitis of the adjacent vertebra,sub-acute bacterial

endocarditis, bronchiectasis.


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Toxic.

Clinical features-It occurs over several days to 2-3 weeks.It is

common in the mid- or low- thoracic region,It presents as back

pain, progressive para-paresis, paresthesia ascending from the

lower limbs to the hands.Sensory loss is cpommon below thelevel.Bladder involvement occurs in the form of retention

initially, then presents as automatic bladder, deep reflexes are

exaggerated and trophic changes over the back and skin in the

form of edema and bed sores.

Management

- CSF shows 5-50 lymphocytes/mm3 .

- care of the skin, bladder, etc.

- high protein diet supplemented with vitamins.- Physiotherapy, psychotherapy.

SACD - Associated with pernicious anemia.

-subjective sensory disturbances paresthesia, etc.

- objective sensory loss- vibration,joint position loss in

glove-and-stocking areas.

- Muscle weakness.

- Sensory ataxia- Rombergs sign.- Deep tendon reflexes variable because of super-

imposed picture of peripheral neuropathy.

- Optic atrophy, dementia.

Multiple Sclerosis-

Common in young adult females.

Occurs due to the de-myelination of CNS-Different sites

and a picture of remissions and exacerbations.

Due to genetic per-disposition and viral infection- auto-

immune mechanism, ? lipid metabolism abnormality.

Clinical features-

1) Sudden onset paresis of the lower limbs.

2) diplopia, vertigo and ataxia.


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3)Trigeminal neuralgia.

4)Unilateral retro-bulbar optic neuritis.

CSF- increased proteins-oligo-clonal, VER-abnormal,

CT/MRI.

Treatment- steroids.

Tabes dorsalis- involves the posterior root and column.

Pain- lightning, fixed crisis; the patient has a sensation of

walking on cotton wool.

Sensory- butterfly area oss over the face, loss over the

insides of the arm, saddle area and feet.

Syringomyelia-there is obstruction to the foramina of thefourth ventricle and is associated with anomalies of the

cranio-vertebral junction ( herniation of the cerebellar

tonsils through the foramen magnum, spina bifida, kypho-

scoliosis).

The spinal cord is enlarged in the transverse plane in the

lower cervical and upper thoracic area.There is a cavity

containing clear fluid occupying the anterior gray column

anterior to the central canal leading to anterior horn cellcompression, and later the compression of the ascending and

descending tracts.

Clinical features

- Asymmetric hypotonia, wasting and weakness of the

small muscles of the hand.

- Loss of the pain and temperature sensation ( due to

involvement of the decussating fibers), touch

unimpaired.- Ocular sympathetic involvement- Horners

syndrome.

Degenerative disorders-

Friedreichs ataxia


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Hereditary spastic ataxia.(Marie)

Hereditary areflexic dysstasia ( Roussy-Levy)

Olivo-ponto-cerebellar atrophy.

MND

Abeta-lipoproteinemia.

central nervous system-theory

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