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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)
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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IPSILATERAL (medial syndromes)
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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IPSILATERAL (medial syndromes)
Medial midpontine syndrome(paramedian branch ofmidbasilar artery)
Ataxia of limbs and gait (moreprominent in bilateralinvolvement): Pontine nuclei
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IPSILATERAL (medial syndromes)
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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IPSILATERAL (medial syndromes)
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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IPSILATERAL (lateral syndromes)
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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Lateral superior pontine syndrome
(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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IPSILATERAL (lateral syndromes)
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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IPSILATERAL (lateral syndromes)
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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IPSILATERAL (lateral syndromes)
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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CONTRALATERAL (medial
syndromes)
Medial midbrain syndrome(paramedian branches of upperbasilar and proximal posterior
cerebral arteries) Paralysis of face, arm, and leg:
Corticobulbar and corticospinal
tract descending in crus cerebri
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CONTRALATERAL (medial
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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CONTRALATERAL (medial
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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CONTRALATERAL (medial
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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CONTRALATERAL (medial
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
dilated and unresponsive pupil:Third nerve fibers
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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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Medial inferior pontine syndrome
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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Lateral inferior pontine syndrome
On side opposite lesion
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
On side opposite lesion
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
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
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
On side opposite lesion
Hemiataxia, hyperkinesias, tremor: Red nucleus,dentatorubrothalamic pathway
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Lateral superior pontine syndrome
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
Lateral midbrain syndrome
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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
Lateral inferior pontine syndrome
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Lateral inferior pontine syndrome
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
Medial midbrain syndrome
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
Medial inferior pontine syndrome
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Medial inferior pontine syndrome
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
On side opposite lesion
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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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11/07/11 MUN FP Academic Half Day 135
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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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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
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
Spinal Cord SyndromeSpinal Cord Syndrome
Spinal Cord SyndromeSpinal Cord Syndrome
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)
Spinal Cord SyndromeSpinal Cord Syndrome
Spinal Cord SyndromeSpinal Cord Syndrome
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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
Spinal Cord SyndromeSpinal Cord Syndrome
Spinal Cord SyndromeSpinal Cord Syndrome
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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