cns diseases1

8/6/2019 cns diseases1

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11/07/11 MUN FP Academic Half Day 1

Definition Of Stroke

Rapidly developed clinical sign offocal disturbance of cerebral functionof presumed vascular origin and ofmore than 24 hours WHO

TIA (Transient Ischemic Attack)recovery is complete within 24

hours. 10% of patients will go on tohave a stroke.


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Sub-types Of Stroke

Ischemic obstruction to one ofmajor cerebral arteries, brainstemstrokes are less common.

Haemorrhage 9% are caused byhaemorrhage to the deep parts ofthe brain. Patients are usually

hypertensive.


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Common Causes

Thrombosis Lacunar stroke (small vessel)

Large vessel thrombosis

Dehydration


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Causes of Ischemic Stroke

Embolic occlusion

Artery-to-artery

Carotid bifurcation

Aortic arch

Arterial dissection


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Cardio embolic

causes of Ischemic Stroke

Atrial fibrillation

Mural thrombus

Myocardial infarction

Dilated cardiomyopathy

Valvular lesions

Mitral stenosis

Mechanical valveBacterial endocarditis


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Causes of Ischemic Stroke

Paradoxical embolus

Atrial septal defect

Patent foramen ovaleAtrial septal aneurysm

Spontaneous echo contrast


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Uncommon Causes

Hypercoaguable disordersProtein C deficiency

Protein S deficiency

Antithrombin III deficiency

Antiphospholipid syndrome

Factor V Leiden mutationa

Prothrombin G20210 mutationaSystemic malignancy


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Uncommon Causes

Sickle cell anemia

-Thalassemia

Polycythemia vera

Systemic lupus erythematosus

Homocysteinemia Thrombotic thrombocytopenic purpura

Disseminated intravascular coagulation

Dysproteinemias

Nephrotic syndrome

Inflammatory bowel disease Oral contraceptives


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Uncommon Causes

Venous sinuous thrombosis

Fibro muscular dysplasia

Vasculitis Systemic vasculitis (PAN, Wegener's,

Takayasu's, giant cell arteritis)

Primary CNS vasculitis

Meningitis (syphilis, tuberculosis,

fungal, bacterial, zoster)


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Uncommon Causes

CardiogenicMitral valve calcificationAtrial myxoma Intracardiac tumorMarantic endocarditis Libman-Sacks endocarditis

Subarachnoid hemorrhage vasospasmDrugs: cocaine, amphetamine

Moyamoya disease Eclampsia


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Fibro muscular dysplasia

Affects the cervical arteries andoccurs mainly in women.

The carotid or vertebral arteries showmultiple rings of segmentalnarrowing alternating with dilatation.

Occlusion is usually incomplete. The process is often asymptomatic

but occasionally is associated with an

audible bruit, TIAs, or stroke. Involvement of the renal arteries iscommon and may result inhypertension.


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Moyamoya disease

Occlusive disease

Large intracranial arteries, especially thedistal internal carotid artery and the stemof the MCA and ACA

Vascular inflammation is absent.

"Puff of smoke" (moyamoya in Japanese)on conventional x-ray angiography.


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"Puff of smoke" (moyamoya in

Japanese)

The lenticulostriate arteries developa rich collateral circulation aroundthe occlusive lesion, which gives the

impression of a "Puff of smoke"(Moyamoya in Japanese)

Other collaterals include

Transdural anastomoses betweenthe cortical surface branches of themeningeal and scalp arteries.


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AVMs

AVMs occur in all parts of the cerebralhemispheres, brainstem, and spinalcord,

Largest ones are most frequently inthe posterior half of the hemispheres,commonly forming a wedge-shapedlesion extending from the cortex to

the ventricle. Present from birth in most patients,


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Bleeding or other symptoms

Most common between the ages

of 10 and 30, occasionally aslate as the fifties.

AVMs are more frequent in men,and rare familial cases have

been described.


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AVMs

Headache (without bleeding) may behemicranial and throbbing, like migraine, ordiffuse.

Focal seizures, with or without

generalization, occur in ~30% of cases. Half of AVMs become evident asintracerebral hemorrhages.

In most, the hemorrhage is mainlyintraparenchymal with extension into thesubarachnoid space in some cases.


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AVMs complications

The risk of rerupture is ~24%per year and is particular high inthe first few weeks.

Hemorrhages may be massive,leading to death, or may be assmall as 1 cm in diameter,

leading to minor focalsymptoms or no deficit.


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steal blood

The AVM may be large enough tosteal blood away from adjacentnormal brain tissue or to increase

venous pressure significantly toproduce venous ischemia locally andin remote areas of the brain.

This is seen most often with large

AVMs in the territory of the MCA.


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Large AVMs of the anterior

circulation

Systolic and diastolic bruit(sometimes self-audible) overthe eye, forehead, or neck

Bounding carotid pulse.


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Silent

Headache at the onset of AVMrupture is not generally asexplosive as with aneurysmalrupture.


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Imageology

MRI is better than CT fordiagnosis, although noncontrastCT scanning sometimes detectscalcification of the AVM andcontrast may demonstrate theabnormal blood vessels.


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Future

The impact of recurrenthemorrhage on disability isrelatively modest, so the

indication for Surgery in asymptomatic AVMs

is debated A large-scale randomized trial is

currently addressing thisquestion.


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FIGURE 3.11. Non-contrast brain CTscan showing massive intraventricu-lar haemorrhage withhydrocephalus as well aswidespread subarachnoidhaemorrhage. The patient was aged

45 years and suddenly slumped ontop of his wife during intercourse.


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FIGURE 3.15. Digital subtractionangiogram showing a left middlecerebral artery aneurysm (arrow).


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CT scan of a 31-year-old male withsud- den right hemiplegia andaltered level of consciousness,showing a large left basalganglia/internal capsularhaemorrhage. Note the movement

artefacts as the patient was restlessand not fully co-operative.


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Medial

PMB of upper basilar andproximal Posterior CerebralArtery

PMB of UBA

PMB of MBA

PMB of basilar artery

Occlusion of VA or of branch ofvertebral or LBA


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Lateral

Small penetrating arteries arisingfrom PCA

Syndrome of superior Cerebellar

artery SCFA (short circumferential artery)

AICA

PICA, Superior, middle, or inferiorbranches of lateral medullary artery,vertebral artery


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Midbrain syndrome:

Medial

Paramedian branches of upper

basilar and proximal posteriorcerebral arteries

Lateral

Syndrome of small penetratingarteries arising from posteriorcerebral artery


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Superior pontine syndrome

Medial (paramedian branches ofupper basilar artery)

Lateral (syndrome of superiorCerebellar artery)


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Middle pontine syndrome

Medial midpontine syndrome(paramedian branch ofmidbasilar artery)

Lateral midpontine syndrome(short circumferential artery)


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Inferior pontine syndrome

Medial (occlusion of paramedianbranch of basilar artery)

Lateral (occlusion of anteriorinferior Cerebellar artery)


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Medullary syndrome

Medial (occlusion of vertebralartery or of branch of vertebralor lower basilar artery)

Lateral (occlusion of any of fivevessels may be responsiblevertebral, posterior inferiorCerebellar, superior, middle, or

inferior lateral medullaryarteries)


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IPSILATERAL

Medial midbrain syndrome(paramedian branches of upperbasilar and proximal posterior

cerebral arteries) Eye "down and out" secondary

to unopposed action of fourthand sixth cranial nerves, with

dilated and unresponsive pupil:Third nerve fibers


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Lateral midbrain syndrome

Lateral midbrain syndrome (syndrome ofsmall penetrating arteries arising fromposterior cerebral artery)

Eye "down and out" secondary to unopposed

action of fourth and sixth cranial nerves,with dilated and unresponsive pupil: Thirdnerve fibers and/or third nerve nucleus

On side opposite lesion Hemiataxia, hyperkinesias, tremor: Red

nucleus, dentatorubrothalamic pathway


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IPSILATERAL (medial syndromes)


cerebral arteries) Eye "down and out" secondary

to unopposed action of fourthand sixth cranial nerves, with



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Medial superior pontine syndrome(paramedian branches of upper basilarartery)

Cerebellar ataxia (probably): Superior

and/or middle Cerebellar peduncle Internuclear ophthalmoplegia: Medial

longitudinal fasciculus Myoclonic syndrome, palate, pharynx, vocal

cords, respiratory apparatus, face,

oculomotor apparatus, etc.: Localizationuncertaincentral tegmental bundle,dentate projection, inferior olivary nucleus


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Medial midpontine syndrome(paramedian branch ofmidbasilar artery)

Ataxia of limbs and gait (moreprominent in bilateralinvolvement): Pontine nuclei


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Medial inferior pontine syndrome(occlusion of paramedian branch ofbasilar artery)

Paralysis of conjugate gaze to side of

lesion (preservation of convergence):Center for conjugate lateral gaze

Nystagmus: Vestibular nucleus Ataxia of limbs and gait: Likely

middle Cerebellar peduncle Diplopia on lateral gaze:Abducens

nerve


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Medial medullary syndrome(occlusion of vertebral artery orof branch of vertebral or lower

basilar artery) Paralysis with atrophy of half

the tongue:Ipsilateral twelfth

nerve


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IPSILATERAL (lateral syndromes)

Lateral midbrain syndrome (syndrome ofsmall penetrating arteries arising fromposterior cerebral artery)

Eye "down and out" secondary to unopposed

action of fourth and sixth cranial nerves,with dilated and unresponsive pupil: Thirdnerve fibers and/or third nerve nucleus

On side opposite lesion Hemiataxia, hyperkinesias, tremor: Red

nucleus, dentatorubrothalamic pathway


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Lateral superior pontine syndrome(syndrome of superior Cerebellarartery)

Ataxia of limbs and gait, falling toside of lesion: Middle and superiorCerebellar peduncles, superior

surface of cerebellum, dentatenucleus

Dizziness, nausea, vomiting;horizontal nystagmus: Vestibularnucleus

Lateral superior pontine syndrome


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(syndrome of superior Cerebellar artery)

Paresis of conjugate gaze(ipsilateral): Pontine contralateral

gaze Skew deviation: Uncertain Miosis, ptosis, decreased sweating

over face (Horner's syndrome):Descending sympathetic fibers

Tremor: Localization unclearDentate nucleus, superior cerebellarpeduncle


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Lateral midpontine syndrome (shortcircumferential artery)

Ataxia of limbs: Middle Cerebellar

peduncle Paralysis of muscles of mastication:

Motor fibers or nucleus of fifth nerve

Impaired sensation over side of face:

Sensory fibers or nucleus of fifthnerve


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Lateral inferior pontinesyndrome (occlusion of anteriorinferior Cerebellar artery)

Horizontal and verticalnystagmus, vertigo, nausea,vomiting, oscillopsia: Vestibular

nerve or nucleus Facial paralysis: Seventh nerve

Lateral inferior pontine syndrome (occlusion of


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Lateral inferior pontine syndrome (occlusion of

anterior inferior Cerebellar artery)

Paralysis of conjugate gaze to side oflesion: Center for conjugate lateral

gaze Deafness, tinnitus:Auditory nerve or

cochlear nucleus Ataxia: Middle Cerebellar peduncle

and Cerebellar hemisphere Impaired sensation over face:

Descending tract and nucleus fifthnerve


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Lateral medullary syndrome(occlusion of any of five vessels maybe responsiblevertebral, posterior

inferior Cerebellar, superior, middle,or inferior lateral medullary arteries)

Pain, numbness, impaired sensationover half the face: Descending tract

and nucleus fifth nerve


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LMS

Ataxia of limbs, falling to side oflesion: Uncertainrestiform body,Cerebellar hemisphere, Cerebellar

fibers, spinocerebellar tract (?) Nystagmus, diplopia, oscillopsia,

vertigo, nausea, vomiting:

Vestibular nucleus


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LMS

Horner's syndrome (miosis, ptosis,decreased sweating): Descending

sympathetic tract

Dysphagia, hoarseness, paralysis ofpalate, paralysis of vocal cord,diminished gag reflex:Issuing fibersninth and tenth nerves

Loss of taste: Nucleus and tractussolitarius


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LMS

Numbness of ipsilateral arm,trunk, or leg: Cuneate andgracile nuclei

Weakness of lower face:Genuflected upper motor neuronfibers to ipsilateral facial

nucleus


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CONTRALATERAL (medial

syndromes)


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syndromes)


cerebral arteries) Paralysis of face, arm, and leg:

Corticobulbar and corticospinal

tract descending in crus cerebri


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syndromes)

Medial superior pontine syndrome(paramedian branches of upperbasilar artery)

Paralysis of face, arm, and leg:Corticobulbar and corticospinal tract

Rarely touch, vibration, and positionare affected: Medial lemniscus


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syndromes)

Medial midpontine syndrome(paramedian branch of midbasilarartery)

Paralysis of face, arm, and leg:Corticobulbar and corticospinal tract

Variable impaired touch andproprioception when lesion extends

posteriorly: Medial lemniscus

CO (


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syndromes)

Medial inferior pontine syndrome(occlusion of paramedian branch ofbasilar artery)

Paralysis of face, arm, and leg:Corticobulbar and corticospinal tractin lower Pons

Impaired tactile and proprioceptive

sense over half of the body: Mediallemniscus

CONTRALATERAL ( di l


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syndromes)

Medial medullary syndrome(occlusion of vertebral artery or ofbranch of vertebral or lower basilar

artery) Paralysis of arm and leg, sparing

face; impaired tactile andproprioceptive sense over half the

body: Contralateral pyramidal tractand medial lemniscus

CONTRALATERAL


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CONTRALATERAL

(Lateral syndromes)

Lateral midbrain syndrome(syndrome of small penetratingarteries arising from posterior

cerebral artery) Hemiataxia, hyperkinesias,

tremor: Red nucleus,

dentatorubrothalamic pathway

CONTRALATERAL


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CONTRALATERAL

(Lateral syndromes)

Lateral superior pontine syndrome(syndrome of superior Cerebellarartery)

Impaired pain and thermal sense onface, limbs, and trunk: Spinothalamictract

Impaired touch, vibration, andposition sense, more in leg than arm

(there is a tendency to incongruity ofpain and touch deficits): Mediallemniscus (lateral portion)

CONTRALATERAL


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CONTRALATERAL

(Lateral syndromes)

Lateral midpontine syndrome(short circumferential artery)

Impaired pain and thermalsense on limbs and trunk:Spinothalamic tract

CONTRALATERAL


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CONTRALATERAL

(Lateral syndromes)

Lateral inferior pontinesyndrome (occlusion of anteriorinferior Cerebellar artery)

Impaired pain and thermalsense over half the body (mayinclude face): Spinothalamic

tract

CONTRALATERAL


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CONTRALATERAL

(Lateral syndromes)

Lateral medullary syndrome(occlusion of any of five vessels maybe responsiblevertebral, posterior

inferior Cerebellar, superior, middle,or inferior lateral medullary arteries)

Impaired pain and thermal senseover half the body, sometimes face:

Spinothalamic tract


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Lateral midpontine syndrome:Impaired pain and thermal sense onlimbs and trunk: Spinothalamic tract

Lateral inferior pontine syndrome

:Impaired pain and thermal senseover half the body (may includeface): Spinothalamic tract

Lateral medullary syndrome :Impaired pain and thermal sense

over half the body, sometimes face:Spinothalamic tract


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Medial midbrain syndrome

(paramedian branches of upperbasilar and proximal posteriorcerebral arteries)

Eye "down and out" secondaryto unopposed action of fourthand sixth cranial nerves, with



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Lacunar infarcts


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Lacunar infarcts

Lacunar infarcts are small infarcts inthe deeper parts of the brain (basalganglia, thalamus, white matter)

and in the brain stem. They are responsible for about 20

percent of all strokes.

Lacunar infarcts


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Lacunar infarcts

Other names given to this pathologyare

Small artery arteriosclerosis",

Hyaline atreriolosclerosis",

Lipohyalinosis".


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Lacunar infarcts


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Lacunar infarcts

They are caused by occlusion of deeppenetrating branches of major cerebralarteries and are particularly common inhypertension and diabetes, which areassociated with severe atherosclerosis ofsmall vessels and small vessel disease

A small lacunar infarct (e.g., one involvingthe internal capsule) can cause as severe aneurological deficit as can a much largerhemispheric infarct but without the life-

threatening cerebral edema that is seen inthe latter.


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Embolic occlusion

Artery-to-artery Carotid bifurcation

Aortic arch

Arterial dissection

Cardioembolic


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Cardioembolic

Atrial fibrillation

Mural thrombus

Myocardial infarction

Dilated cardiomyopathy

Valvular lesions

Mitral stenosis

Mechanical valve Bacterial endocarditis

Paradoxical embolus

Atrial septal defect

Patent foramen ovale

Atrial septal aneurysm

Spontaneous echo contrast


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Cardiogenic


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Cardiogenic

CardiogenicMitral valve calcification Atrial myxoma Intracardiac tumor

Marantic endocarditis Libman-Sacks endocarditis

Subarachnoid hemorrhage vasospasmDrugs: cocaine, amphetamine

Moyamoya disease Eclampsia


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Medial Medullary syndrome

Occlusion of vertebral artery or ofbranch of vertebral or lower basilarartery

On side of lesion

Paralysis with atrophy of half the tongue:Ipsilateral twelfth nerve

On side opposite lesion Paralysis of arm and leg, sparing face;

impaired tactile and proprioceptive senseover half the body: Contra lateralpyramidal tract and medial lemniscus


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Lateral Medullary syndrome

Dysphagia, hoarseness, paralysis of palate,paralysis of vocal cord, diminished gag reflex:

Issuing fibers ninth and tenth nerves Loss of taste: Nucleus and Tractus Solitarius

Numbness of ipsilateral arm, trunk, or leg:Cuneate and Gracile nuclei Weakness of lower face: Genuflectedupper motor

neuron fibers to ipsilateral facial nucleus On side opposite lesion Impaired pain and thermal sense over half the

body, sometimes face: Spinothalamic tract


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Basilar artery syndrome

The syndrome of the lone vertebralartery is equivalent: A combination ofthe various brainstem syndromesplus those arising in the posterior

cerebral artery distribution. Bilateral long tract signs (sensory andmotor; Cerebellar and peripheral cranialnerve abnormalities): Bilateral long tract;Cerebellar and peripheral cranial nerves

Paralysis or weakness of all extremities,plus all bulbar musculature: Corticobulbarand corticospinal tracts bilaterally


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Medial inferior pontine syndrome

Occlusion of Para median branch ofbasilar artery

On side of lesion Paralysis of conjugate gaze to side of

lesion (preservation of convergence):Center for conjugate lateral gaze

Nystagmus: Vestibular nucleus Ataxia of limbs and gait: Likely Middle

Cerebellar Peduncle Diplopia on lateral gaze:Abducens

nerve


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On side opposite lesion

Paralysis of face, arm, and leg:Corticobulbar and corticospinal

tract in lower Pons Impaired tactile and proprioceptive

sense over half of the body: Medial

lemniscus


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Impaired pain and thermal senseover half the body (may include

face): Spinothalamic tract


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Medial mid pontine syndrome

Medial midpontine syndrome (paramedianbranch of midbasilar artery)

On side of lesion Ataxia of limbs and gait (more prominent

in bilateral involvement): Pontine nuclei On side opposite lesion Paralysis of face, arm, and leg:

Corticobulbar and corticospinal tract

Variable impaired touch andproprioception when lesion extendsposteriorly: Medial lemniscus


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Lateral mid pontine syndrome

Lateral mid pontine syndrome (shortcircumferential artery)

On side of lesion Ataxia of limbs: Middle cerebellar peduncle

Paralysis of muscles of mastication: Motor fibersor nucleus of fifth nerve

Impaired sensation over side of face: Sensoryfibers or nucleus of fifth nerve


Impaired pain and thermal sense on limbs andtrunk: Spinothalamic tract


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Medial superior pontine syndrome

Medial superior pontine syndrome (paramedianbranches of upper basilar artery) On side of lesion

Cerebellar ataxia (probably): Superior and/or middlecerebellar peduncle

Internuclear ophthalmoplegia: Medial longitudinal

fasciculus Myoclonic syndrome, palate, pharynx, vocal cords,respiratory apparatus, face, oculomotor apparatus,etc.: Localization uncertaincentral tegmental bundle,dentate projection, inferior olivary nucleus

On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and

corticospinal tract

Rarely touch, vibration, and position are affected:Medial lemniscus


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Medial midbrain syndrome (paramedianbranches of upper basilar and proximalposterior cerebral arteries) On side of lesion

Eye "down and out" secondary to unopposedaction of fourth and sixth cranial nerves, withdilated and unresponsive pupil: Third nervefibers

On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar

and corticospinal tract descending in cruscerebri


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Lateral midbrain syndrome (syndrome ofsmall penetrating arteries arising fromposterior cerebral artery) On side of lesion

Eye "down and out" secondary to unopposedaction of fourth and sixth cranial nerves, withdilated and unresponsive pupil: Third nerve fibersand/or third nerve nucleus


Hemiataxia, hyperkinesias, tremor: Red nucleus,dentatorubrothalamic pathway


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On side opposite lesion Impaired pain and thermal sense on

face, limbs, and trunk: Spinothalamictract

Impaired touch, vibration, and positionsense, more in leg than arm (there is atendency to incongruity of pain andtouch deficits): Medial lemniscus (lateralportion)

Intravenous Recombinant Tissue


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Plasminogen Activator

Indication Clinical diagnosis of stroke

Onset of symptoms to time of drugadministration 3 h

CT scan showing no hemorrhage oredema of > of the MCA territory

Age 18 years

Consent by patient or surrogate

Contraindication


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Sustained BP >185/110 despite treatment Platelets


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Medial brain stem syndromes

1. Medial midbrain syndrome paramedian branches ofupper basilar and proximal

posterior cerebral arteries 3. Medial superior pontine syndrome Paramedian branches ofupper basilar artery 4. Medial midpontine syndrome Paramedian branch ofmidbasilar artery 5. Medial inferior pontine syndrome Occlusion of paramedian branch ofbasilar artery 9. Medial Medullary syndrome Occlusion ofvertebral artery or of branch of

vertebral or lower basilar artery


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Lateral brain stem syndromes

2. Lateral midbrain syndrome Syndrome ofsmall penetrating arteries arising from

posterior cerebral artery 6. Lateral superior pontine syndrome Syndrome ofsuperior Cerebellar artery 7. Lateral midpontine syndrome Short circumferential artery 8. Lateral inferior pontine syndrome Occlusion ofanterior inferior Cerebellar artery Lateral medullary syndrome: Occlusion of any of five vessels may be responsible

vertebral, posterior inferior Cerebellar, superior,

middle, or inferior lateral Medullary arteries


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Medial brain stem syndromes

Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract descending in crus cerebri Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract Rarely touch, vibration, and position are affected Medial lemniscus Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract

Variable impaired touch and proprioception when lesion extends posteriorly: Medial lemniscus Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract in lower Pons Impaired tactile and proprioceptive sense over half of the body: Medial lemniscus Paralysis of arm and leg, sparing face; impaired tactile and proprioceptive

sense over half the body: Contra lateral pyramidal tract and medial lemniscus


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Lateral brain stem syndromes

Hemiataxia, hyperkinesias, tremor: Red nucleus, dentatorubrothalamic pathway Impaired pain and thermal sense on face, limbs,

and trunk: Spinothalamic tract Impaired touch, vibration, and position sense, more

in leg than arm (there is a tendency to incongruityof pain and touch deficits): Medial lemniscus(lateral portion)

Impaired pain and thermal sense on limbs andtrunk: Spinothalamic tract

Impaired pain and thermal sense over half the body(may include face): Spinothalamic tract

Impaired pain and thermal sense over half the bodysometimes face: Spinothalamic tract

Lateral Medullary syndrome


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(occlusion of any of five vessels may be responsiblevertebral, posteriorinferior Cerebellar, superior, middle, or inferior lateral Medullary arteries)

On side of lesion 1. Pain, numbness, impaired sensation over half the face: Descending tract and nucleus fifth nerve 2. Ataxia of limbs, falling to side of lesion: Uncertain Restiform body, Cerebellar hemisphere, Cerebellar fibers, spino Cerebellar

tract (?) 3. Nystagmus, diplopia, oscillopsia, vertigo, nausea, vomiting: Vestibular nucleus 4. Horner's syndrome (miosis, ptosis, decreased sweating): Descending sympathetic tract 5. Dysphagia, hoarseness, paralysis of palate, paralysis of vocal cord, diminished gag

reflex: Issuing fibers ninth and tenth nerves 6. Loss of taste: Nucleus and tractus solitarius 7. Numbness of ipsilateral arm, trunk, or leg: Cuneate and gracile nuclei 8. Weakness of lower face: Genuflected upper motor neuron fibers to ipsilateral facial nucleus



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syndrome of small penetrating arteriesarising from posterior cerebral artery

On side of lesion Eye "down and out" secondary to unopposed

action of fourth and sixth cranial nerves, withdilated and unresponsive pupil: Third nerve fibers and/or third nerve

nucleus On side opposite lesion

Hemiataxia, hyperkinesias, tremor: Red nucleus, dentatorubrothalamic pathway

Lateral superior pontine syndrome (syndrome of


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ate a supe o po t e sy d o e (sy d o e o

superior Cerebellar artery)

On side of lesion Ataxia of limbs and gait, falling to side of lesion: Middle and superior Cerebellar peduncles, superior surface of cerebellum,

dentate nucleus Dizziness, nausea, vomiting; horizontal Nystagmus: Vestibular nucleus Paresis of conjugate gaze (ipsilateral):

Pontine contra lateral gaze 4. Skew deviation: Uncertain 5. Miosis, ptosis, decreased sweating over face (Horner's syndrome): Descending sympathetic fibers 6. Tremor: Localization unclear Dentate nucleus, superior Cerebellar peduncle On side opposite lesion Impaired pain and thermal sense on face, limbs, and trunk: Spinothalamic tract Impaired touch, vibration, and position sense, more in leg than arm (there is a

tendency to incongruity of pain and touch deficits): Medial lemniscus (lateral portion)

Lateral midpontine syndrome


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Short circumferential artery

On side of lesion 1. Ataxia of limbs: Middle Cerebellar

peduncle 2. Paralysis of muscles of mastication:

Motor fibers or nucleus of fifth nerve 3. Impaired sensation over side of face: Sensory fibers or nucleus of fifth

nerve

On side opposite lesion Impaired pain and thermal sense on limbsand trunk: Spinothalamic tract



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occlusion of anterior inferior Cerebellar artery

On side of lesion 1.Horizontal and vertical Nystagmus, vertigo, nausea,

vomiting, oscillopsia: Vestibular nerve or nucleus 2.Facial paralysis: Seventh nerve Paralysis of conjugate gaze to side of lesion: Center

for conjugate lateral gaze 3.Deafness, tinnitus:Auditory nerve or cochlearnucleus

4.Ataxia: Middle Cerebellar peduncle andCerebellar hemisphere

5.Impaired sensation over face: Descending tractand nucleus fifth nerve

On side opposite lesion Impaired pain and thermal sense over half the body

(may include face): Spinothalamic tract

Medial Medullary syndrome

Occlusion of vertebral artery or of branch of vertebral or lower

basilar artery


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basilar artery

On side of lesion

Paralysis with atrophy of half the tongue:Ipsilateral twelfth nerve

On side opposite lesion Paralysis of arm and leg, sparing face;

impaired tactile and proprioceptive senseover half the body:

Contra lateral pyramidal tract andmedial lemniscus


paramedian branches of upper basilar and proximal posterior

cerebral arteries


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cerebral arteries

On side of lesion Eye "down and out" secondary to

unopposed action of fourth and sixthcranial nerves, with dilated and

unresponsive pupil: Third nerve fibers On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract

descending in crus cerebri

Medial superior pontine syndrome

(paramedian branches of upper basilar artery)


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(paramedian branches of upper basilar artery)

On side of lesion 1. Cerebellar ataxia (probably): Superior and/or middle Cerebellar peduncle 2. Internuclear ophthalmoplegia: Medial longitudinal fasciculus 3. Myoclonic syndrome, palate, pharynx, vocal cords,

respiratory apparatus, face, oculomotor apparatus, etc.:Localization uncertain

central tegmental bundle, dentate projection, inferiorolivary nucleus

On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and

corticospinal tract Rarely touch, vibration, and position are affected: Medial lemniscus

Medial midpontine syndrome

Paramedian branch of midbasilar artery


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Paramedian branch of midbasilar artery

On side of lesion Ataxia of limbs and gait (more prominent

in bilateral involvement): Pontine nuclei On side opposite lesion Paralysis of face, arm, and leg:

Corticobulbar and corticospinal tract Variable impaired touch and

proprioception when lesion extendsposteriorly: Medial lemniscus



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occlusion of paramedian branch of basilar artery

On side of lesion 1.Paralysis of conjugate gaze to side of lesion

(preservation of convergence): Center for conjugate lateral gaze 2.Nystagmus: Vestibular nucleus 3.Ataxia of limbs and gait: Likely middle

Cerebellar peduncle 4.Diplopia on lateral gaze:Abducens nerve On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar

and corticospinal tract in lower Pons Impaired tactile and proprioceptive sense over

half of the body: Medial lemniscus



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1. Medial midbrain syndrome paramedian branches of upper basilar and

proximal posterior cerebral arteries Paralysis of face, arm, and leg:

Corticobulbar and corticospinal tractdescending in crus cerebri 2. Lateral midbrain syndrome Syndrome of small penetrating arteries

arising from posterior cerebral artery

Hemiataxia, hyperkinesias, tremor: Red nucleus, dentatorubrothalamic pathway

M di l ti d


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Medial pontine syndromes

3. Medial superior pontine syndrome (Paramedian branches of upper basilar artery) Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract Rarely touch, vibration, and position are affected Medial lemniscus 4. Medial midpontine syndrome Paramedian branch of midbasilar artery

Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract Variable impaired touch and proprioception when lesion extends posteriorly: Medial lemniscus 5. Medial inferior pontine syndrome (Occlusion of paramedian branch of basilar artery) Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract in lower Pons Impaired tactile and proprioceptive sense over half of the body:

Medial lemniscus

L t l ti d


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Lateral pontine syndromes

6. Lateral superior pontine syndrome (Syndrome of superior Cerebellar artery) Impaired pain and thermal sense on face, limbs, and trunk: Spinothalamic tract Impaired touch, vibration, and position sense, more in leg than

arm (there is a tendency to incongruity of pain and touchdeficits):

Medial lemniscus (lateral portion) 7. Lateral midpontine syndrome Short circumferential artery Impaired pain and thermal sense on limbs and trunk: Spinothalamic tract 8. Lateral inferior pontine syndrome (occlusion of anterior

inferior Cerebellar artery)

Impaired pain and thermal sense over half the body (mayinclude face): Spinothalamic tract

Contra lateral


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Contra lateral

9. Medial Medullary syndrome Occlusion of vertebral artery or of branch of vertebral

or lower basilar artery Paralysis of arm and leg, sparing face; impaired tactile

and proprioceptive sense over half the body: Contra lateral pyramidal tract and medial lemniscus

10. Lateral medullary syndrome: (Occlusion of any of five vessels may be responsible

vertebral, posterior inferior Cerebellar, superior,middle, or inferior lateral Medullary arteries)

Impaired pain and thermal sense over half the bodysometimes face:

Spinothalamic tract

BRAIN STEM SYNDROMES


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BRAIN-STEM SYNDROMES

WEBER (ANTERIOR CEREBRALPEDUNCLE MIDBRAIN)IL3+CL7UMN+CLHP

CLAUDE; CEREBRAL PEDUNCLEINVOLVING RED NUCLEUS IL3 + CLCEREBELLAR SIGNS

PARINAUD;


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PARINAUD;

DORSAL MB/ TECTUM

VERTICAL GAZE PALSY+

CONVERGENCE DISORDERS +

CONVERGENCE RETRACTION+

NYSTAGMUS+

PUPILLARY & LID DISORDERS


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WALLENBERG;LATERAL MEDULLARY

SYNDROME


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SYNDROME;

IL5,7,9,10,11+IL HONER+ILCEREBELLAR+

CL SPINOTHALAMIC

VESTIBULAR DISTURBANCE.

Vernet 9 10 11


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Vernet 9,10,11

Jugular foramen (inside the skull)

Metastases, neurinoma,meningioma, Epidermoid & carotid

body tumor.

Collet Sicard 9 10 11 12


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Collet Sicard 9,10,11,12

Jugular foramen (out side the skullnear foramen lacerum)

Metastases, neurinoma,

meningioma, Epidermoid & carotidbody tumor.

Villaret 9 10 11 12 & Horner's


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Villaret 9,10,11,12 & Horner s

Posterior retropharyngeal spacenear carotid artery

Carotid dissection, Metastases,

neurinoma, meningioma,Epidermoid & carotid body tumor.


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Haemophilus Influenzae type b (Hib)


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Meningococcus Pneumococcus

MeningococcusMening

ococcus


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MeningococcusMeningococcus

common organisms that cause meningitis inchildren.

caused by bacteria called Neisseria meningitidis.

There are several strains of Neisseriameningitidis.

Strain BStrain B causes about 75 percent of themeningococcal cases and has the highest fatalityfatalityrate.rate.


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Haemophilus Influenzae type B (Hib)Haemophilus Influenzae type B (Hib)

is caused by haemophilus bacteria. It

was once the most common form ofbacterial meningitis,

one of the deadliest childhooddeadliest childhooddiseases.

PneumococcusPneumococcus


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PneumococcusPneumococcus

is caused bypneumococcus bacteria,which also cause several diseases of therespiratory system, including

pneumonia. It has a fatality rate of about 20 percent.

It also results in a higher incidence of

brain damagebrain damage than other forms of thedisease.

SymptomsSy

mptoms


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SymptomsSymptoms

Symptoms of meningitis can come on very quickly or take a couple of days to

appear. Most cases ofmeningitis occur in the first 5 years of lifemeningitis occur in the first 5 years of life, with the peak

incidence between 3 and 5 monthsbetween 3 and 5 months of age.

Older people:


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Older people:

1. Lethargy2. Recurring headaches

3. Difficulty in concentration

4. Short-term memory loss

5. Clumsiness

6. Balance problems

7. Depression

Serious complicationsSerious comp

lications


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Serious complicationsSe ous co p ca o s

Other seriouscomplications caninclude:

1. Brain damage

1. Epilepsy

2. Changes in eye sight

SUMMARYSUMMARY


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SUMMARY

Meningitis is an inflammation of theprotective membrane lining the brainand spinal cord caused most often by aviral or bacterial infection that crossesthe body's blood-brain barrier.

Meningitis is diagnosed by a lumbarpuncture , in which a small amount offluid is collected from the spinalcolumn.

There are two main types of

meningitis: bacterial and viral.Bacterial meningitis is less common,but more serious.

SUMMARYSUMMARY


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SU

Bacterial meningitis is treated with antibiotics and themajority of patients make a full recovery.

Viral meningitis usually requires no treatment beyondpainkillers.

Most patients make a full recovery from meningitis. Asmall number of infected people end up with hearing or

vision loss or brain damage. Vaccinations against some forms of meningitis are

available. They are recommended for children under age5, people in close contact with someone who hasdeveloped meningitis, college students, and peopletraveling to certain overseas destinations.


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11/07/11 MUN FP Academic Half Day 159Clin Microbiol Infect 2003;9;803-809


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11/07/11 MUN FP Academic Half Day 160 Clin Microbiol Infect 2003;9;803-809

PREDISPOSING FACTORS


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IVDA (2.5%)

Congenital heart disease (6.1%)

HIV infection (1.2%)

Immunosuppression (3.7%)

Diabetes mellitus (3.1%)

Stages


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g

1. Early cerebritis stage (D1-3):focal area ofinflammation and edema

2. Late cerebritis stage (D4-9):development of anecrotic central focus

3. Early capsule stage (D10-14):ring-enhancing

capsule of well-vascularized tissue with earlyappearance of peripheral fibrosis

4. Late capsule stage (>D14):host defenses lead toa well-formed capsule

~Clin Infect Dis. 1997 Oct;25(4):763-79


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IMAGING STUDIES


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2. MRI

T1: hypointense with ring-enhancement

T2: hyperintense central area of pussurrounded by a well-defined hypointensecapsule & edema-> surgery

3. Radionuclide scan

D/D brain abscess from tumor


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CerebellumCerebellumFunctionFunction

CerebellumCerebellumFunctionFunction


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11/07/11 MUN FP Academic Half Day

Maintenance of EquilibriumMaintenance of Equilibrium - balance, posture, eye movement- balance, posture, eye movement

Coordination of half-automatic movement ofCoordination of half-automatic movement ofwalking and posture maintenacewalking and posture maintenace- posture, gait- posture, gait

Adjustment of Muscle ToneAdjustment of Muscle Tone

Motor Leaning Motor SkillsMotor Leaning Motor SkillsCognitive FunctionCognitive Function

Motor SkillMotor Skill


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Motor SkillMotor Skill

Pablo CasalsPablo CasalsPablo CasalsPablo Casals

CerebellumCerebellum ClinicalClinicalSyndromesSyndromes

CerebellumCerebellum ClinicalClinicalSyndromesSyndromes


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AtaxiaAtaxia: incoordination of movement: incoordination of movement - decomposition of movement- decomposition of movement

- dysmetria, past-pointing- dysmetria, past-pointing

- dysdiadochokinesia- dysdiadochokinesia

- rebound phenomenon of Holmes- rebound phenomenon of Holmes- gait ataxia, truncal ataxia, titubation- gait ataxia, truncal ataxia, titubation

IntentionIntention TremorTremor

Hypotonia,Hypotonia, NystagmusNystagmus

Archicerebellar LesionArchicerebellar Lesion: medulloblastoma: medulloblastomaPaleocerebellar LesionPaleocerebellar Lesion: gait disturbance: gait disturbance

Neocerebellar LesionNeocerebellar Lesion: hypotonia, ataxia, tremor: hypotonia, ataxia, tremor

CerebellarCerebellara b c


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CerebellarCerebellar

AtaxiaAtaxia

Ataxic gait andAtaxic gait and

position:position:

Left cerebellar tumorLeft cerebellar tumor

a. Sways to the right ina. Sways to the right in

standing positionstanding position

b. Steady on theb. Steady on the

right legright leg

c. Unsteady on thec. Unsteady on the

left legleft leg

d. ataxic gaitd. ataxic gait

d

CerebellarCerebellar


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Cerebellar tumors onCerebellar tumors on vermisvermis

- Truncal Ataxia- Truncal Ataxia

- Frequent Falling- Frequent Falling

The child in this picture:The child in this picture:

- would not try to stand- would not try to stand

unsupportedunsupported- would not let go of the bed rail- would not let go of the bed rail

if she was stood on the floor.if she was stood on the floor.

MedulloblastomaMedulloblastoma


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BalanceBalance

What is Multiple Sclerosis?What is Multiple Sclerosis?


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It is an Auto Immune Diseasewhich is when the body starts todestroy itself.

It is a life-long disease with no

cure. In MS, the body attacks anddestroys the fatty tissue calledmyelin that insulates anaxon/nerve, and is calleddemyelination.

What is Multiple Sclerosis?


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Multiple Sclerosis (MS) is an chronicinflammatory demyelinating diseaseof the brain and spinal cord.

The Human Nervous System


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Areas affected byMS Brain

Spinal cord

Optic nerves

(http://web.lemoyne.edu/~hevern/psy340/lectures/psy340.04.2.ns.structure.html)

Initial Presentation of MS


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Incidence(%)

Optic nerve inflammation 1429

Poor balance (ataxia) 218

Dizziness (vertigo) 29

Weakness 1040

Double visions (diplopia) 818

Bladder, bowel dysfunction 014

Pain 2140

Sensory loss 1339

Other Common Symptoms of MS


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FatigueSpasticity

Sexual dysfunction

Cognitive impairmentGenerally occurs later in thedisease

Multiple Sclerosis Clinical SubtypesMultiple Sclerosis Clinical Subtypes

Relapsing-remitting Secondary-progressive


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Lublin FD et al. Neurology. 1996;46:907-911.

p g g

Primary-progressive

Dis

abilit

y

Time

Time

Dis

abilit

y

y p g

Progressive-relapsing

Time

Time

Dis

abilit

y

Dis

abilit

y

How Is MS Diagnosed?


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At least two episodes of symptomsOccur at different points in time

Result from involvement of different areas

of the central nervous system Absence of other treatable causes for

the symptoms

Results of neurological testing

Other Potential Causes of

MS-like Symptoms


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Lyme disease

Lupus

Migraine

Non-recurrent inflammatory process Encephalitis

Stroke

Tumor of the brain or spinal cord

Brain Atrophy (Shrinkage)

in Untreated MS


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Images acquired over the course of 7 years

from a single person with untreated MS

Brain Atrophy (Shrinkage)

in Untreated MS


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Treatment of New MS Exacerbations


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Drug therapyCorticosteroids

Intravenous immunoglobulin

Plasma exchange Physical therapy


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Glatiramer

acetate

Prevention of Future Attacks and

Disease Progression


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Immune modulating drugsBeta-Interferon

Glatiramer acetate

Humanized monoclonal antibodies Immunosuppressant drugs

Anti-cancer agents

Combination therapies

Symptom Management Examples


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Pain control

Management of impaired bladderand bowel function

Anti-spasmodic drugs Treatment of fatigue

Splinting for contractures

Counseling

MS Therapies: What Lies Ahead?


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Neural protection Regenerative therapies

Cell replacement (stem cells)

Dietary approaches (vitamin D)

Multiple SclerosisMultiple Sclerosis


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If damage is severe it can also destroy the nerve/axonitself.

MS affects the central nervous system and inflamesthe white matter in the brain which creates plaques.White matter is below the top layer of our brain andspinal cord. Plaques block a signal from being passedfrom the body to the spinal cord and brain.

Currently in the US, 250,000-300,000 people havebeen diagnosed with MS and there are 200 new casesdiagnosed every week.

Diagnostic categories of MS


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The phrase multiple abnormalitiesin space and time sums up what aphysician needs to find a diagnosis

of MS (OConnor 32). There are three categories of MS;

Definite, Probable, and Possible MS.

Possible MS:


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There is no documented signsof MS and more than onelesion.

There is also a history of onerelapse-remitting symptoms.


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Definite MS:


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Consistent course (relapse-remittingcourse with at least 2 bouts separated by atleast 1 month or

slow or stepwise progressive course for at

least 6 months) of documented neurologicalsigns of lesions in more than one site ofbrain or spinal cord white matter ( Hope7).

The age of onset is between 10 and 50

years of age.

Symptoms of MSSymptoms of MS


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Fatigue Depression

Memory change

Pain

Spasticity Vertigo

Tremor

Double Vision/Vision

Loss

Weakness Dizziness/Unsteadines

s

Numbness/Tingling

Ataxia Euphoria

Speech disturbance

Bladder/Bowel/Sexualdysfunction

Medications used for MSMedications used for MS


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Spasticity- Baclofen, Tizanidine, Diazepam, Dantrolene Optic Neuritis-Methlyprednisolone, Oral steroids Fatigue-Antidepressant, Amantadine

Pain-Codeine, Aspirin

Sexual Dysfunction-Viagra, Pravatine Tremor-Isoniazid, Primidone, Propranolol Disease-Modifying Drugs- Interferon beta 1a and

1b, and Glatiramer acetate

Interferon Beta 1b(Betaseron):


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Is slightly different from our own interferon. This medication does the same thing as beta 1a,

but is injected just under the skin every twodays.

Side effects include irritation, bruising, and

redness at the site of injection and the flu likesymptoms. This is also given to people whohave definite progressive MS.

Disease-Modifying DrugsDisease-Modifying Drugs (cont)(cont)


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Glatiramer Acetate ( Copaxone): is asmall fragment of a protein that resembles a protein in

myelin ( OConnor 106). It decrease the reoccurrence of relapse.

It is injected just under the skin every day.

There is no flu like symptoms but occasional rednessmay occur at the injection site. A few amount of people do experience brief shortness

of breathe.

In summary all three of these drugs decrease relapses

by 33%, have manageable side effect, are injected,stabilize the disease, and tend to be costly.

Parkinson Disease


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Neurological disease affecting over four millionpatients worldwide, over 1.5 million people inthe U.S.. While it can affect individuals at anyage, it is most common in the elderly.

The average age of onset is 55 years, althoughapproximately 10 percent of cases affect thoseunder age 40.


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Clinical Characteristics


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James Parkinson, 1917 ...involuntary tremulous motion, with lessened muscular power, in parts

not in action and even when supported; with a propensity to bend the

trunk forwards, and to pass from a walking to a funning pace, the senses

and the intellects uninjured.

rhythmic tremor at rest rigidity with cog-wheel characteristic

akinesia


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ETIOLOGY

Genetic Factors


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1999 - examined 17,000 twins

> 50 years old: no genetic effect

< 50 years old: 10 % genetic defect

Diet vitamins, antioxidants incidenceSmoking incidenceEnvironment incidence in rural areas

dopamine neuron toxins

Normal

Pathophysiology of Parkinsons Disease


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STRIATUM

PALLIDUM

SUBSTANTA

NIGRA

THALAMUS

MOTOR

CORTEX

Pathology

STRIATUM

PALLIDUMSUBSTANTA

NIGRATHALAMUS

MOTORCORTEX

STAGES OF PARKINSON'S DISEASE

DOPAMINE

(% control)


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(% control)

ADAPTIVECAPACITY

0

20

40

60

80

100

DECOMPENSATION

COMPENSATION

-no symptoms

MILD SYMPTOMS

MARKED SYMPTOMS

Levodopa therapy


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Main treatment is with L-DOPAPrecursor for dopamine

Sinemet is L-DOPA + carbidopacarbidopa is a peripheral decarboxylase inhibitor

- prevents L-DOPA catabolism Main problems:

- on/off fluctuations- dyskinesias

- eventually doesnt work- peripheral side effects (NE and E)

Anticholinergics help as well On-off fluctuations too great with DA agonists

Drugs used to treat Parkinsons Disease


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Appears Later in Life

Continuous Progressive

Neurological Disease, therebycausing increasing disability ofmovement

no cure

Etiology


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Cerebral atherosclerosis

Viral encephalitis

Side effects of severalantipsychotic drugs (i.e.,phenothiazides, butyrophenones,

reserpine)

Environmental factors and neurotoxins


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Pesticides, herbicides, industrialchemicals - contain substancesthat inhibit complex I in the

mitochondria


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In Terms of Etiology and Clinical Picture, Major

Symptoms Involve:


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Bradykinesia- Slowness in Initiation andExecution of Voluntary Movements

Rigidity - Increase Muscle Tone andIncrease Resistance to Movement (Armsand Legs Stiff)

Tremor - Usually Tremor at Rest, WhenPerson Sits, Arm Shakes, Tremor StopsWhen Person Attempts to Grab Something

Postural Instability - abnormal fixation ofposture (stoop when standing), equilibrium,and righting reflex

Gait Disturbance - Shuffling Feet

Usually Other Accompanied Autonomic

Deficits Seen Later in Disease Process:


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Orthostatic Hypotension Dementia

Dystonia

Ophthalmoplegia Affective Disorders


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The Dopaminergic Neurons in the Basal Ganglia Aremainly affected

Acetylcholine within striatum is a tonically activatedneuron

It impinges on GABA Neuron by an Excitatory Action

GABA Neuron Has an Inhibitory Action on theSubstantia Nigra from Substantia Nigra, Has aDopaminergic Feed Back Loop Back to Striatum

Which Gets Loss Giving Signs and Symptoms ofParkinson Disease

Basal Ganglia


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The Basal Ganglia Consists of Five LargeSubcortical Nuclei That Participate inControl of Movement:

Caudate Nucleus

Putamen

Globus Pallidus

Subthalamic Nucleus

Substantia Nigra

The balance of the five large Subcortical Nuclei are

responsible for smooth motor movements


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The primary input is from the Cerebral Cortex,and the output Is directed through the thalamusback to the Prefrontal, Premotor, and MotorCortex

The motor function of the basal ganglia aretherefore mediated by the Frontal Cortex

Neurotransmitters in Basal Ganglia IncludeSerotonin, Acetylcholine, GABA, Enkephalin,Substance P, Glutamate, and Dopamine

Dopamine from Substantia Nigra decreasesrelease of acetylcholine from striatum.


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Agents that Increase Dopamine

functions Increasing the synthesis of dopamine - l-


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Increasing the synthesis of dopamine - l-Dopa

Inhibiting the catabolism of dopamine -selegiline

Stimulating the release of dopamine -amphetamine

Stimulating the dopamine receptor sitesdirectly - bromocriptine & pramipexole

Blocking the uptake and enhancing therelease of dopamine - amantadine


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L Dopa Therapy for ParkinsonDisease


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Dopamine DecarboxylaseConverts L Dopa to DopamineThat Gets Stored into Secretory

Vesicles and Gets Releasedfrom Basal Ganglia

Effects of L Dopa on the Symptoms of

Parkinson Disease


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L Dopa Fairly Effective in Eliminating Most ofthe Symptoms of Parkinson Disease

Bradykinesia and Rigidity Quickly Respond toL Dopa

Reduction in Tremor Effect with ContinuedTherapy

L Dopa less Effective in Eliminating PosturalInstability and Shuffling Gait Meaning Other

Neurotransmitters Are Involved in ParkinsonDisease

Long Term Therapy

Behavioral Disturbances in 20 to 25% of Population


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Trouble in Thinking (Cognitive Effects) L Dopa Can Induce:

Psychosis

Confusion

Hallucination Anxiety

Delusion

Some Individuals develop Hypomania Which IsInappropriate Sexual Behavior; "Dirty Old Man",

"Flashers"

"On/off" Effect


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"On/off" Effect Is like a Light Switch ; WithoutWarning, All of a Sudden, Person Goes fromFull Control to Complete Reversion Back toBradykinesia, Tremor, Etc. Lasting from 30Minutes to Several Hours and Then Get Control

Again "On/off" Effect Occurs after usually after 2 or

more years on L Dopa

Related to Denervation Hypersensitivity


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Bromocriptine


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For Treating Parkinson Disease ; anErgotamine derivative, acts as aDopamine Receptor Agonist theDrug Produces Little Response inPatients That Do Not React toLevodopa


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Pramipexole

Pramipexole


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Pramipexole is a nonergot dopamine agonistwith high relative in vitrospecificity and fullintrinsicactivity at the D

2subfamily of dopamine

receptors, binding with higher affinity to D3than

to D2 or D4receptor subtypes.

Precise mechanism ofaction is unknown,although it is believed to be related to its abilityto stimulate dopamine receptors in the striatum.

Amantadine
http://defwindow%28%27agonist%27%29/http://defwindow%28%27specificity%27%29/http://defwindow%28%27intrinsic%27%29/http://defwindow%28%27activity%27%29/http://defwindow%28%27affinity%27%29/http://defwindow%28%27receptor%27%29/http://defwindow%28%27mechanism%27%29/http://defwindow%28%27action%27%29/http://defwindow%28%27stimulate%27%29/http://defwindow%28%27stimulate%27%29/http://defwindow%28%27action%27%29/http://defwindow%28%27mechanism%27%29/http://defwindow%28%27receptor%27%29/http://defwindow%28%27affinity%27%29/http://defwindow%28%27activity%27%29/http://defwindow%28%27intrinsic%27%29/http://defwindow%28%27specificity%27%29/http://defwindow%28%27agonist%27%29/


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Amantadine for Treating ParkinsonDisease

Amantadine Effective as in theTreatment of Influenza, however hassignificant Antiparkinson Action; itappears to Enhance Synthesis,Release, or Reuptake of Dopamine

from the Surviving Nigral Neurons

Deprenyl ( Selegiline)


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Deprenyl ( Selegiline) for TreatingParkinson Disease

Deprenyl Selectively InhibitsMonoamine Oxidase B WhichMetabolizes Dopamine, but Does NotInhibit Monoamine Oxidase a WhichMetabolizes Norepinephrine and

Serotonin

The Protective Effects of Selegiline


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Although the factors responsible for the loss of

nigrostriatal dopaminergic neurons in Parkinson's

disease are not understood, the findings from

neurochemical studies have suggested that thesurviving striatal dopamine neurons accelerate the

synthesis of dopamine, thus enhancing the

formation of H202 according to the following

scheme.

Amphetamine for Treating Parkinson

Disease


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Amphetamine Has Been UsedAdjunctively in the Treatment ofSome Parkinsonian Patients it IsThought That, by ReleasingDopamine and Norepinephrine fromStorage Granules, AmphetamineMakes Patients More Mobile and

More Motivated

Catechol-O-methyltransferase (COMT)

inhibitors


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Tolcapone (Tasmar) and Entacapone (Comtan) aretwo well-studied COMT inhibitors.

Increases the duration of effect of levodopa dose

Can increase peak levels of levodopa

Should be taken with carbidopa/levodopa (not effective

used alone) Can be most beneficial in treating "wearing off" responses

Can reduce carbidopa/levodopa dose by 20-30%

Antimuscarinic Agents for Treating

Parkinson Disease


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The Antimuscarinic Agents Are Muchless Efficacious than Levodopa, andThese Drugs Play Only an AdjuvantRole in Antiparkinson Therapy theActions of Atropine, Scopolamine,Benztropine, Trihexyphenidyl, andBiperiden Are Similar

On the Horizon A number of potential Parkinson's treatments in research laboratories

now show much promise. They include:


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Neurotrophic proteins--These appear to protect nerve cells fromthe premature death that prompts Parkinson's. One hurdle isgetting the proteins past the blood-brain barrier.

Neuroprotective agents--Researchers are examining naturallyoccurring enzymes that appear to deactivate "free radicals,"chemicals some scientists think may be linked to the damage doneto nerve cells in Parkinson's and other neurological disorders.

Spinal Cord TractsSpinal Cord Tracts

Spinal Cord TractsSpinal Cord Tracts


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Ascending TractsAscendingTracts

Posterior White Column-Medial Lemniscal PathwayPosterior White Column-Medial Lemniscal Pathway

Spinothalamic TractSpinothalamic Tract

Spinoreticular or Spinoreticulothalamic TractSpinoreticular or Spinoreticulothalamic Tract

Spinocerebellar TractSpinocerebellar Tract

Spinomedullothalamic TractSpinomedullothalamic Tract

Cervicothalamic or Spinocervicothalamic TractCervicothalamic or Spinocervicothalamic TractSpino-olivary TractSpino-olivary Tract

Spinotectal TractSpinotectal Tract

Ascending TractsAscendingTracts

Posterior White Column-Medial Lemniscal PathwayPosterior White Column-Medial Lemniscal Pathway

Spinothalamic TractSpinothalamic Tract

Spinoreticular or Spinoreticulothalamic TractSpinoreticular or Spinoreticulothalamic Tract

Spinocerebellar TractSpinocerebellar Tract

Spinomedullothalamic TractSpinomedullothalamic Tract

Cervicothalamic or Spinocervicothalamic TractCervicothalamic or Spinocervicothalamic Tract

Spino-olivary TractSpino-olivary Tract

Spinotectal TractSpinotectal Tract

Descending Tracts from Brain StemDescending

Tracts from Brain Stem

Descending Tracts from Brain StemDescending

Tracts from Brain Stem

Spinal Cord Descending TractsSpinal Cord Descending Tracts

Spinal Cord Descending TractsSpinal Cord Descending Tracts


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Dorsolateral (Motor) PathwayDorsolateral (Motor) Pathway

Rubrospinal TractRubrospinal Tract

Ventromedial (Motor) PathwayVentromedial (Motor) Pathway

Tectospinal TractTectospinal TractVestibulospinal TractVestibulospinal Tract

MLF (Medial Longitudinal Fasciculus)MLF (Medial Longitudinal Fasciculus)

- interstitiospinal tract- interstitiospinal tract

Sensory Modulation pathwaysSensory Modulation pathwaysRaphespinal & Cerulospinal PathwaysRaphespinal & Cerulospinal Pathways

Descending Autonomic PathwaysDescending Autonomic Pathways

Dorsolateral (Motor) PathwayDorsolateral (Motor) Pathway

Rubrospinal TractRubrospinal Tract

Ventromedial (Motor) PathwayVentromedial (Motor) Pathway

Tectospinal TractTectospinal TractVestibulospinal TractVestibulospinal Tract

MLF (Medial Longitudinal Fasciculus)MLF (Medial Longitudinal Fasciculus)

- interstitiospinal tract- interstitiospinal tract

Sensory Modulation pathwaysSensory Modulation pathwaysRaphespinal & Cerulospinal PathwaysRaphespinal & Cerulospinal Pathways

Descending Autonomic PathwaysDescending Autonomic Pathways

Upper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) SyndromeUpper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) Syndrome

UMN syndromeUMN syndrome LMN SyndromeLMN Syndrome


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Type of ParalysisType of Paralysis Spastic ParesisSpastic Paresis Flaccid ParalysisFlaccid Paralysis

AtrophyAtrophy No (Disuse) AtrophyNo (Disuse) Atrophy SevereSevereAtrophyAtrophy

Deep Tendon ReflexDeep Tendon Reflex IncreaseIncrease Absent DTRAbsent DTR

Pathological ReflexPathological Reflex PositivePositive BabinskiBabinskiSignSign AbsentAbsent

Superficial ReflexSuperficial Reflex AbsentAbsent PresentPresent

Fasciculation andFasciculation and AbsentAbsent Could beCould be

FibrillationFibrillation PresentPresent

Spinal Cord SyndromeSpinal Cord Syndrome



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Predominantly Motor SyndromesPredominantlyMotor Syndromes

Poliomyelitis (Infantile Paralysis)Poliomyelitis (Infantile Paralysis)

- viral infection of lower motor neuron- viral infection of lower motor neuron

- LMN syndrome at the level of lesion- LMN syndrome at the level of lesion

Amyotrophic Lateral Sclerosis (ALS)Amyotrophic Lateral Sclerosis (ALS)

- combined LMN and UMN lesion- combined LMN and UMN lesion

- LMN syndrome at the level of lesion- LMN syndrome at the level of lesion

- UMN syndrome below the level of lesion- UMN syndrome below the level of lesion

- Lou Gehrigs disease- Lou Gehrigs disease



Predominantly

Sensory Syndromes


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Predominantly Sensory Syndromesy y y

Herpes ZosterHerpes Zoster

- inflammatory reactions of spinal ganglion- inflammatory reactions of spinal ganglion

- severe pain on the dermatomes of affected ganglion- severe pain on the dermatomes of affected ganglion

Tabes DorsalisTabes Dorsalis- common variety of neurosyphilis- common variety of neurosyphilis

- posterior column and spinal posterior root lesion- posterior column and spinal posterior root lesion

- loss of discriminative touch sensation and conscious- loss of discriminative touch sensation and consciousproprioception below the level of lesionproprioception below the level of lesion

- posterior column ataxia- posterior column ataxia

- lancinating pain (- lancinating pain (a stabbing or piercing sensationa stabbing or piercing sensation))

- loss of deep tendon reflex (DTR)- loss of deep tendon reflex (DTR)




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Sub-Acute Combined DegenerationSub-Acute Combined Degeneration

(Combined System Disease)(Combined System Disease)

LesionLesion

- posterior white column- posterior white column- corticospinal tract (UMN)- corticospinal tract (UMN)

SymptomSymptom

- loss of discriminative touch sensation and conscious- loss of discriminative touch sensation and conscious

proprioception below the level of lesionproprioception below the level of lesion- ipsilateral UMN syndrome below the level of lesion- ipsilateral UMN syndrome below the level of lesion




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Syringomyelia, HematomyeliaSyringomyelia, HematomyeliaLesionLesion

- central canal of spinal cord- central canal of spinal cord

- gradually extended to peripheral part of the cord- gradually extended to peripheral part of the cord

SymptomSymptom

- initial symptom is bilateral loss of pain- initial symptom is bilateral loss of pain

(compression of anterior white commissure)(compression of anterior white commissure)

- variety of symptoms appear- variety of symptoms appearaccording to the lesion extended from central canalaccording to the lesion extended from central canal


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Interferon Beta 1a (Avonexand Rebif):


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Is a protein that is a replica of humaninterferon. It suppress the immune system and

helps to maintain the blood-brainbarrier.

You inject Avonex into the muscle oncea week and Rebif is injected under theskin three times a week. This drug isuseful to people who have definiteprogressive MS.

One side effect of the drug is a flu likesymptom.

Courses of MSCourses of MS


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Relapse-remitting MS (RRMS):

h k


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Here have an attack, go intocomplete or partial remission, thenhave the symptoms return.

Primary-progressive MS (PPMS):

H i ll d li d h


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Here continually decline and have noremissions.

There may be a temporary relief insymptoms.

A few patients have malignant MSwhich is where they have a quickdecline which leaves them severely

disabled or even lead to death.

Secondary-progressive MS (SPMS):

Thi f MS i h RRMS


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This stage of MS starts with RRMSsymptoms and continues on toshow signs of PPMS.

Progressive-relapsing MS (PRMS):

Thi i f b t h it t k

cns diseases1

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