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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.
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