Definition of Stroke: 11/07/11 MUN FP Academic Half Day 1

Definition Of Stroke
Rapidly developed clinical sign of focal disturbance of cerebral function of presumed vascular origin and of more than 24 hours WHO TIA (Transient Ischemic Attack) recovery is complete within 24 hours. 10% of patients will go on to have a stroke.
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MUN FP Academic Half Day
Sub-types Of Stroke
Ischemic obstruction to one of major cerebral arteries, brainstem strokes are less common. Haemorrhage 9% are caused by haemorrhage to the deep parts of the 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 valve Bacterial endocarditis
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Paradoxical
embolus Atrial septal defect Patent foramen ovale Atrial septal aneurysm Spontaneous echo contrast
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Uncommon Causes
Hypercoaguable
disorders Protein C deficiency Protein S deficiency Antithrombin III deficiency Antiphospholipid syndrome Factor V Leiden mutationa Prothrombin G20210 mutationa Systemic 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
Cardiogenic
Mitral valve calcification Atrial myxoma Intracardiac tumor Marantic endocarditis Libman-Sacks endocarditis
Subarachnoid hemorrhage vasospasm Drugs: cocaine, amphetamine Moyamoya disease Eclampsia
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Fibro muscular dysplasia

Affects the cervical arteries and occurs mainly in women. The carotid or vertebral arteries show multiple rings of segmental narrowing 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 is common and may result in hypertension.
MUN FP Academic Half Day 11
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Moyamoya disease

Occlusive disease Large intracranial arteries, especially the distal internal carotid artery and the stem of 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 develop a rich collateral circulation around the occlusive lesion, which gives the impression of a "Puff of smoke" (Moyamoya in Japanese) Other collaterals include Transdural anastomoses between the cortical surface branches of the meningeal and scalp arteries.
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AVMs
AVMs occur in all parts of the cerebral hemispheres, brainstem, and spinal cord, Largest ones are most frequently in the posterior half of the hemispheres, commonly forming a wedge-shaped lesion 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 as late 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 be hemicranial and throbbing, like migraine, or diffuse. Focal seizures, with or without generalization, occur in ~30% of cases. Half of AVMs become evident as intracerebral hemorrhages. In most, the hemorrhage is mainly intraparenchymal with extension into the subarachnoid space in some cases.
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AVMs complications
The risk of rerupture is ~24% per year and is particular high in the first few weeks. Hemorrhages may be massive, leading to death, or may be as small as 1 cm in diameter, leading to minor focal symptoms or no deficit.
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steal blood
The AVM may be large enough to steal blood away from adjacent normal brain tissue or to increase venous pressure significantly to produce venous ischemia locally and in 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) over the eye, forehead, or neck Bounding carotid pulse.
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Silent
Headache at the onset of AVM rupture is not generally as explosive as with aneurysmal rupture.
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Imageology
MRI is better than CT for diagnosis, although noncontrast CT scanning sometimes detects calcification of the AVM and contrast may demonstrate the abnormal blood vessels.
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Future
The impact of recurrent hemorrhage on disability is relatively modest, so the indication for Surgery in asymptomatic AVMs is debated A large-scale randomized trial is currently addressing this question.
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FIGURE 3.11. Non-contrast brain CT scan showing massive intraventricular haemorrhage with hydrocephalus as well as widespread subarachnoid haemorrhage. The patient was aged 45 years and suddenly slumped on top of his wife during intercourse.
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FIGURE 3.15. Digital subtraction angiogram showing a left middle cerebral artery aneurysm (arrow).
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CT scan of a 31-year-old male with sudden right hemiplegia and altered level of consciousness, showing a large left basal ganglia/internal capsular haemorrhage. Note the movement artefacts as the patient was restless and not fully co-operative.
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Medial
PMB of upper basilar and proximal Posterior Cerebral Artery PMB of UBA PMB of MBA PMB of basilar artery Occlusion of VA or of branch of vertebral or LBA
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Lateral
Small penetrating arteries arising from PCA Syndrome of superior Cerebellar artery SCFA (short circumferential artery) AICA PICA, Superior, middle, or inferior branches of lateral medullary artery, vertebral artery
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Midbrain syndrome:
Medial Paramedian branches of upper basilar and proximal posterior cerebral arteries Lateral Syndrome of small penetrating arteries arising from posterior cerebral artery
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Superior pontine syndrome
Medial (paramedian branches of upper basilar artery) Lateral (syndrome of superior Cerebellar artery)
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Middle pontine syndrome
Medial midpontine syndrome (paramedian branch of midbasilar artery) Lateral midpontine syndrome (short circumferential artery)
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Inferior pontine syndrome
Medial (occlusion of paramedian branch of basilar artery) Lateral (occlusion of anterior inferior Cerebellar artery)
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Medullary syndrome
Medial (occlusion of vertebral artery or of branch of vertebral or lower basilar artery) Lateral (occlusion of any of five vessels may be responsible vertebral, posterior inferior Cerebellar, superior, middle, or inferior lateral medullary arteries)
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IPSILATERAL
Medial midbrain syndrome (paramedian branches of upper basilar and proximal posterior cerebral arteries) Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers
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Lateral midbrain syndrome
Lateral midbrain syndrome (syndrome of small penetrating arteries arising from posterior cerebral artery) Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve 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 upper basilar and proximal posterior cerebral arteries) Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers
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Medial superior pontine syndrome (paramedian branches of upper basilar artery) 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.: Localization uncertaincentral tegmental bundle, dentate projection, inferior olivary nucleus
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Medial midpontine syndrome (paramedian branch of midbasilar artery) Ataxia of limbs and gait (more prominent in bilateral involvement): Pontine nuclei
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Medial inferior pontine syndrome (occlusion of paramedian branch of basilar 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 or of 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 of small penetrating arteries arising from posterior cerebral artery) Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve 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 Cerebellar artery) 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
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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 unclear Dentate nucleus, superior cerebellar peduncle
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Lateral midpontine syndrome (short circumferential 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 fifth nerve
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Lateral inferior pontine syndrome (occlusion of anterior inferior Cerebellar artery) Horizontal and vertical nystagmus, vertigo, nausea, vomiting, oscillopsia: Vestibular nerve or nucleus Facial paralysis: Seventh nerve
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Lateral inferior pontine syndrome (occlusion of anterior inferior Cerebellar artery)
Paralysis of conjugate gaze to side of lesion: 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 fifth nerve
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Lateral medullary syndrome (occlusion of any of five vessels may be responsiblevertebral, posterior inferior Cerebellar, superior, middle, or inferior lateral medullary arteries) Pain, numbness, impaired sensation over half the face: Descending tract and nucleus fifth nerve
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LMS
Ataxia of limbs, falling to side of lesion: 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 of palate, paralysis of vocal cord, diminished gag reflex: Issuing fibers ninth and tenth nerves Loss of taste: Nucleus and tractus solitarius
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LMS
Numbness of ipsilateral arm, trunk, or leg: Cuneate and gracile nuclei Weakness of lower face: Genuflected upper motor neuron fibers to ipsilateral facial nucleus
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CONTRALATERAL (medial syndromes)
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Medial midbrain syndrome (paramedian branches of upper basilar and proximal posterior cerebral arteries) Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract descending in crus cerebri
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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
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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
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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
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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: Contralateral pyramidal tract and medial lemniscus
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CONTRALATERAL (Lateral syndromes)
Lateral midbrain syndrome (syndrome of small penetrating arteries arising from posterior cerebral artery) Hemiataxia, hyperkinesias, tremor: Red nucleus, dentatorubrothalamic pathway
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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 touch deficits): Medial lemniscus (lateral portion)
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Lateral midpontine syndrome (short circumferential artery) Impaired pain and thermal sense on limbs and trunk: Spinothalamic tract
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Lateral inferior pontine syndrome (occlusion of anterior inferior Cerebellar artery) Impaired pain and thermal sense over half the body (may include face): Spinothalamic tract
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Lateral medullary syndrome (occlusion of any of five vessels may be responsiblevertebral, posterior inferior Cerebellar, superior, middle, or inferior lateral medullary arteries) Impaired pain and thermal sense over half the body, sometimes face: Spinothalamic tract
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Lateral midpontine syndrome: Impaired pain and thermal sense on limbs and trunk: Spinothalamic tract Lateral inferior pontine syndrome :Impaired pain and thermal sense over half the body (may include face): 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 upper basilar and proximal posterior cerebral arteries) Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers
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Lacunar infarcts
Lacunar infarcts are small infarcts in the deeper parts of the brain (basal ganglia, thalamus, white matter) and in the brain stem. They are responsible for about 20 percent of all strokes.
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Lacunar infarcts
Other names given to this pathology are Small artery arteriosclerosis", Hyaline atreriolosclerosis", Lipohyalinosis".
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Lacunar infarcts are caused by small vessel disease.
This nonspecific term refers to a vascular lesion seen primarily in hypertension and diabetes but occurring also in old age.
Other names given to this pathology are "small artery arteriosclerosis", "hyaline atreriolosclerosis", and "lipohyalinosis". This change affects small penetrating arteries and arterioles that originate from the base of the brain and supply the basal ganglia, thalamus, deep white matter, and the brainstem.
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Lacunar infarcts
They are caused by occlusion of deep penetrating branches of major cerebral arteries and are particularly common in hypertension and diabetes, which are associated with severe atherosclerosis of small vessels and small vessel disease A small lacunar infarct (e.g., one involving the internal capsule) can cause as severe a neurological deficit as can a much larger hemispheric infarct but without the lifethreatening cerebral edema that is seen in the latter.
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Embolic occlusion
Artery-to-artery
Carotid bifurcation Aortic arch Arterial dissection
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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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Hypercoagulable disorders

Protein C deficiency Protein S deficiency Antithrombin III deficiency Antiphospholipid syndrome Factor V Leiden mutationa Prothrombin G20210 mutationa Systemic malignancy Sickle cell anemia -Thalassemia Polycythemia vera Systemic lupus erythematosus Homocysteinemia Thrombotic thrombocytopenic purpura
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Hypercoaguable disorders

Venous sinous thrombosisb Fibromuscular dysplasia Vasculitis Systemic vasculitis (PAN, Wegener's, Takayasu's, giant cell arteritis) Primary CNS vasculitis Meningitis (syphilis, tuberculosis, fungal, bacterial, zoster)
Disseminated intravascular coagulation Dysproteinemias Nephrotic syndrome Inflammatory bowel disease Oral contraceptives
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Cardiogenic
Cardiogenic
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Medial Medullary syndrome

Occlusion of vertebral artery or of branch of vertebral or lower 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 sense over half the body: Contra lateral pyramidal tract and medial lemniscus
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Lateral Medullary syndrome

Occlusion of any of five vessels may be responsiblevertebral, posterior inferior Cerebellar, superior, middle, or inferior Lateral Medullary arteries On side of lesion Pain, numbness, impaired sensation over half the face: Descending tract and nucleus fifth nerve Ataxia of limbs, falling to side of lesion: Uncertain Restiform body, Cerebellar hemisphere, Cerebellar fibers, Spinocerebellar tract (?) Nystagmus, diplopia, oscillopsia, vertigo, nausea, vomiting: Vestibular nucleus Horner's syndrome (miosis, ptosis, decreased sweating): Descending sympathetic tract
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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: Genuflected upper 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 vertebral artery is equivalent: A combination of the various brainstem syndromes plus those arising in the posterior cerebral artery distribution. Bilateral long tract signs (sensory and motor; Cerebellar and peripheral cranial nerve abnormalities): Bilateral long tract; Cerebellar and peripheral cranial nerves Paralysis or weakness of all extremities, plus all bulbar musculature: Corticobulbar and corticospinal tracts bilaterally
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Medial inferior pontine syndrome

Occlusion of Para median branch of basilar 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

Lateral inferior pontine syndrome (occlusion of anterior inferior cerebellar artery) On side of lesion Horizontal and vertical nystagmus, vertigo, nausea, vomiting, oscillopia: Vestibular nerve or nucleus Facial paralysis: Seventh nerve Paralysis of conjugate gaze to side of lesion: 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 fifth nerve
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Lateral inferior pontine syndrome

On side opposite lesion Impaired pain and thermal sense over half the body (may include face): Spinothalamic tract
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Medial mid pontine syndrome

Medial midpontine syndrome (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 extends posteriorly: Medial lemniscus
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Lateral mid pontine syndrome

Lateral mid pontine syndrome (short circumferential artery) On side of lesion 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 fifth nerve On side opposite lesion Impaired pain and thermal sense on limbs and trunk: Spinothalamic tract
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Medial superior pontine syndrome
Medial superior pontine syndrome (paramedian branches of upper basilar artery)
On side of lesion

On side opposite lesion

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.: Localization uncertaincentral tegmental bundle, dentate projection, inferior olivary nucleus Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract Rarely touch, vibration, and position are affected: Medial lemniscus
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Lateral superior pontine syndrome
Lateral superior pontine syndrome (syndrome of 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 contralateral gaze Skew deviation: Uncertain Miosis, ptosis, decreased sweating over face (Horner's syndrome): Descending sympathetic fibers Tremor: Localization unclearDentate nucleus, superior cerebellar peduncle
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Medial midbrain syndrome
Medial midbrain syndrome (paramedian branches of upper basilar and proximal posterior cerebral arteries)
On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial 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
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Lateral midbrain syndrome (syndrome of small penetrating arteries arising from posterior cerebral artery)
On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve 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

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)
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Intravenous Recombinant Tissue Plasminogen Activator

Indication
Clinical diagnosis of stroke Onset of symptoms to time of drug administration 3 h CT scan showing no hemorrhage or edema of > of the MCA territory Age 18 years Consent by patient or surrogate
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Contraindication

Sustained BP >185/110 despite treatment Platelets <100,000; HCT <25%; glucose <50 or >400 mg/dL Use of heparin within 48 h and prolonged PTT, or elevated INR Rapidly improving symptoms Prior stroke or head injury within 3 months; prior intracranial hemorrhage Major surgery in preceding 14 days Minor stroke symptoms Gastrointestinal bleeding in preceding 21 days Recent myocardial infarction Coma or stupor
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Medial brain stem syndromes

1. Medial midbrain syndrome paramedian branches of upper basilar and proximal posterior cerebral arteries 3. Medial superior pontine syndrome Paramedian branches of upper basilar artery 4. Medial midpontine syndrome Paramedian branch of midbasilar artery 5. Medial inferior pontine syndrome Occlusion of paramedian branch of basilar artery 9. Medial Medullary syndrome Occlusion of vertebral artery or of branch of vertebral or lower basilar artery
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Lateral brain stem syndromes

2. Lateral midbrain syndrome Syndrome of small penetrating arteries arising from posterior cerebral artery 6. Lateral superior pontine syndrome Syndrome of superior Cerebellar artery 7. Lateral midpontine syndrome Short circumferential artery 8. Lateral inferior pontine syndrome Occlusion of anterior 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 incongruity of pain and touch deficits): Medial lemniscus (lateral portion) Impaired pain and thermal sense on limbs and trunk: Spinothalamic tract Impaired pain and thermal sense over half the body (may include face): Spinothalamic tract Impaired pain and thermal sense over half the body sometimes face: Spinothalamic tract
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(occlusion of any of five vessels may be responsiblevertebral, posterior inferior 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 arteries arising from posterior cerebral artery On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve 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 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)
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Lateral midpontine syndrome 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 limbs and trunk: Spinothalamic tract
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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 cochlear nucleus 4.Ataxia: Middle Cerebellar peduncle and Cerebellar hemisphere 5.Impaired sensation over face: Descending tract and nucleus fifth nerve On side opposite lesion Impaired pain and thermal sense over half the body (may include face): Spinothalamic tract
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Medial Medullary syndrome Occlusion of vertebral artery or of branch of vertebral or lower 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 sense over half the body: Contra lateral pyramidal tract and medial lemniscus
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Medial midbrain syndrome paramedian branches of upper basilar and proximal posterior cerebral arteries
On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial 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
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Medial superior pontine syndrome (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, 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 midpontine syndrome 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 extends posteriorly: Medial lemniscus
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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
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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 tract descending in crus cerebri 2. Lateral midbrain syndrome Syndrome of small penetrating arteries arising from posterior cerebral artery Hemiataxia, hyperkinesias, tremor: Red nucleus, dentatorubrothalamic pathway
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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
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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 touch deficits): 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 (may include face): Spinothalamic tract
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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 body sometimes face: Spinothalamic tract
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BRAIN-STEM SYNDROMES
WEBER (ANTERIOR CEREBRAL PEDUNCLE MIDBRAIN) IL3+CL7UMN+CLHP CLAUDE; CEREBRAL PEDUNCLE INVOLVING RED NUCLEUS IL3 + CL CEREBELLAR SIGNS
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PARINAUD;

DORSAL MB/ TECTUM VERTICAL GAZE PALSY+ CONVERGENCE DISORDERS + CONVERGENCE RETRACTION+ NYSTAGMUS+ PUPILLARY & LID DISORDERS
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MILLARD-GUBLAR;

PONTO-MEDULLARY Jn. IL6+IL7LMN CLHP
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WALLENBERG;LATERAL MEDULLARY SYNDROME;
IL5,7,9,10,11+IL HONER+IL CEREBELLAR+ CL SPINOTHALAMIC VESTIBULAR DISTURBANCE.
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Vernet 9,10,11

Jugular foramen (inside the skull) Metastases, neurinoma, meningioma, Epidermoid & carotid body tumor.
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Collet Sicard 9,10,11,12
Jugular foramen (out side the skull near foramen lacerum) Metastases, neurinoma, meningioma, Epidermoid & carotid body tumor.
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Villaret 9,10,11,12 & Horner's
Posterior retropharyngeal space near carotid artery Carotid dissection, Metastases, neurinoma, meningioma, Epidermoid & carotid body tumor.
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Isolated 12th

Skull base (hypoglossal canal) Metastases, neurinoma, meningioma, Epidermoid.
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Caused by virus. Less severe Resolves without specific treatment within a week or two Also called as aseptic meningitis Eg : Enteroviruses (family of viruses)
Caused by bacteria Quite severe and may result in a) brain damage b) hearing loss c) learning disability It would also causes death!
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Haemophilus Influenzae type b (Hib)
Meningococcus
Pneumococcus
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Meningococcus

common organisms that cause meningitis in children. caused by bacteria called Neisseria meningitidis. There are several strains of Neisseria meningitidis. Strain B causes about 75 percent of the meningococcal cases and has the highest fatality rate.
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Haemophilus Influenzae type B (Hib)
is caused by haemophilus bacteria. It was once the most common form of bacterial meningitis, one of the deadliest childhood diseases.
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Pneumococcus
is caused by pneumococcus bacteria, which also cause several diseases of the respiratory system, including pneumonia. It has a fatality rate of about 20 percent. It also results in a higher incidence of brain damage than other forms of the disease.
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Symptoms
Symptoms of meningitis can come on very quickly or take a couple of days to appear. Most cases of meningitis occur in the first 5 years of life, with the peak life incidence between 3 and 5 months of age.
1. 2. 3. 4. 5. 6. 7.
Older people: Lethargy Recurring headaches Difficulty in concentration Short-term memory loss Clumsiness Balance problems Depression
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Serious complications
Other serious complications can include: Brain damage Epilepsy Changes in eye sight
1.
1.
2.
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SUMMARY
Meningitis is an inflammation of the protective membrane lining the brain and spinal cord caused most often by a viral or bacterial infection that crosses the body's blood-brain barrier. Meningitis is diagnosed by a lumbar puncture , in which a small amount of fluid is collected from the spinal column. There are two main types of meningitis: bacterial and viral. Bacterial meningitis is less common, but more serious.
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SUMMARY

Bacterial meningitis is treated with antibiotics and the majority of patients make a full recovery. Viral meningitis usually requires no treatment beyond painkillers. Most patients make a full recovery from meningitis. A small 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 age 5, people in close contact with someone who has developed meningitis, college students, and people traveling to certain overseas destinations.
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Brain Abscess Definition
A focal, intracerebral infection that begins as a localized area of cerebritis ->a collection of pus surrounded by a wellvascularized capsule
~Clin Infect Dis. 1997 Oct;25(4):763-79
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Common Sources of Brain Abscess

1.
2.
3.
4.
Direct or indirect infection from paranasal sinuses, middle ear, and teeth (via valveless emissary veins to cavernous sinus) Penetrating brain injury (low incidence) Metastatic seeding from distant extracranial sources Cryptic (20%~30%) : PFO?
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PREDISPOSING FACTORS

IVDA (2.5%) Congenital heart disease (6.1%) HIV infection (1.2%) Immunosuppression (3.7%) Diabetes mellitus (3.1%)
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Stages
1. Early cerebritis stage (D1-3):focal area of inflammation and edema 2. Late cerebritis stage (D4-9):development of a necrotic central focus 3. Early capsule stage (D10-14):ring-enhancing capsule of well-vascularized tissue with early appearance of peripheral fibrosis 4. Late capsule stage (>D14):host defenses lead to a well-formed capsule ~Clin Infect Dis. 1997 Oct;25(4):763-79
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IMAGING STUDIES
1.
Contrasted CT focal hypodensity->enhances after iv contrast->ring-enhanced lesion Frequently located in watershed areas, regular thin-walled capsule with peripheral enhancement Brain tumor: irregular border & diffuse enhancement
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IMAGING STUDIES
2. MRI T1: hypointense with ring-enhancement T2: hyperintense central area of pus surrounded by a well-defined hypointense capsule & edema-> surgery 3. Radionuclide scan D/D brain abscess from tumor
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Function Function
Cerebellum Cerebellum
Maintenance of Equilibrium - balance, posture, eye movement Coordination of half-automatic movement of walking and posture maintenace - posture, gait Adjustment of Muscle Tone Motor Leaning Motor Skills Cognitive Function
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Motor Skill
Pablo Casals Pablo Casals
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Syndromes Syndromes
Cerebellum Cerebellum
Clinical Clinical
Ataxia: incoordination of movement - decomposition of movement - dysmetria, past-pointing - dysdiadochokinesia - rebound phenomenon of Holmes - gait ataxia, truncal ataxia, titubation Intention Tremor Hypotonia, Nystagmus Archicerebellar Lesion: medulloblastoma Paleocerebellar Lesion: gait disturbance Neocerebellar Lesion: hypotonia, ataxia, tremor
Cerebellar Ataxia
Ataxic gait and position: Left cerebellar tumor a. Sways to the right in standing position b. Steady on the right leg c. Unsteady on the left leg d. ataxic gait
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Cerebellar Medulloblastoma
Cerebellar tumors on vermis - Truncal Ataxia - Frequent Falling The child in this picture: - would not try to stand unsupported - would not let go of the bed rail if she was stood on the floor.
Balance
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What is Multiple Sclerosis?

It is an Auto Immune Disease which is when the body starts to destroy itself. It is a life-long disease with no cure. In MS, the body attacks and destroys the fatty tissue called myelin that insulates an axon/nerve, and is called demyelination.
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What is Multiple Sclerosis?
Multiple Sclerosis (MS) is an chronic inflammatory demyelinating disease of the brain and spinal cord.
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The Human Nervous System
Areas affected by MS

Brain Spinal cord Optic nerves
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Initial Presentation of MS
Optic nerve inflammation Poor balance (ataxia) Dizziness (vertigo) Weakness Double visions (diplopia) Bladder, bowel dysfunction Pain Sensory loss
Incidence (%) 1429 218 29 1040 818 014 2140 1339

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Other Common Symptoms of MS

Fatigue Spasticity Sexual
dysfunction Cognitive impairment

Generally
occurs later in the
disease
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Multiple Sclerosis Clinical Subtypes

Relapsing-remitting Secondary-progressive
Disability
Time Primary-progressive
Disability
Time Progressive-relapsing Time
Disability
Disability
Time
Lublin FD et al. Neurology. 1996;46:907-911.
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How Is MS Diagnosed?
At least two episodes of symptoms

Occur
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
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Other Potential Causes of MS-like Symptoms

Lyme disease Lupus Migraine Non-recurrent inflammatory process Encephalitis Stroke Tumor of the brain or spinal cord
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Brain Atrophy (Shrinkage) in Untreated MS
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
Drug therapy
Corticosteroids Intravenous
immunoglobulin Plasma exchange
Physical therapy
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Glatiramer acetate
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Prevention of Future Attacks and Disease Progression
Immune modulating drugs

Beta-Interferon Glatiramer
acetate Humanized monoclonal antibodies
Immunosuppressant drugs
Anti-cancer
agents
Combination therapies
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Symptom Management Examples

Pain control Management of impaired bladder and bowel function Anti-spasmodic drugs Treatment of fatigue Splinting for contractures Counseling
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MS Therapies: What Lies Ahead?

Neural protection Regenerative therapies Cell replacement (stem cells) Dietary approaches (vitamin D)
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Multiple Sclerosis

If damage is severe it can also destroy the nerve/axon itself. MS affects the central nervous system and inflames the white matter in the brain which creates plaques. White matter is below the top layer of our brain and spinal cord. Plaques block a signal from being passed from the body to the spinal cord and brain. Currently in the US, 250,000-300,000 people have been diagnosed with MS and there are 200 new cases diagnosed every week.
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Diagnostic categories of MS
The phrase multiple abnormalities in space and time sums up what a physician needs to find a diagnosis of MS (OConnor 32). There are three categories of MS; Definite, Probable, and Possible MS.
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Possible MS:
There is no documented signs of MS and more than one lesion. There is also a history of one relapse-remitting symptoms.
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Probable MS:
Here the signs are not previously documented and there is one current sign of MS. There is more than one site of lesions, they have a good recovery and have a history of relapse-remitting symptoms.
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Definite MS:
Consistent course (relapse-remitting course with at least 2 bouts separated by at least 1 month or slow or stepwise progressive course for at least 6 months) of documented neurological signs of lesions in more than one site of brain or spinal cord white matter ( Hope 7). The age of onset is between 10 and 50 years of age.
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Symptoms of MS

Fatigue Depression Memory change Pain Spasticity Vertigo Tremor Double Vision/Vision Loss
Weakness Dizziness/Unsteadines s Numbness/Tingling Ataxia Euphoria Speech disturbance Bladder/Bowel/Sexual dysfunction
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Medications used for MS

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
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Interferon Beta 1b (Betaseron):

Is slightly different from our own interferon. This medication does the same thing as beta 1a, but is injected just under the skin every two days. Side effects include irritation, bruising, and redness at the site of injection and the flu like symptoms. This is also given to people who have definite progressive MS.
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Disease-Modifying Drugs
(cont)
Glatiramer Acetate ( Copaxone): is a small 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 redness may 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.
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Parkinson Disease
Neurological disease affecting over four million patients worldwide, over 1.5 million people in the U.S.. While it can affect individuals at any age, it is most common in the elderly. The average age of onset is 55 years, although approximately 10 percent of cases affect those under age 40.
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Clinical Characteristics
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

Pathology of Parkinson's
Death of Dopamine neurons in the Substantia Nigra Loss of Dopamine in the Caudate Loss of Inhibition in the Caudate Overactive output (globus pallidus) to the thalamus Thalamus over inhibits the motor cortex Complex basal ganglia-cortical loops
EPIDEMIOLOGY
fifth or sixth decade of life 85% idiopathic prevalence: 3 per 1000 cumulative life-time risk: 1 in 40 approximately 1 million patients
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no cure
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ETIOLOGY
Genetic Factors
1999 - examined 17,000 twins > 50 years old: no genetic effect < 50 years old: 10 % genetic defect Diet vitamins, antioxidants incidence
Smoking incidence Environment incidence in rural areas dopamine neuron toxins

Pathophysiology of Parkinsons Disease Normal

STRIATUM
PALLIDUM THALAMUS SUBSTANTA NIGRA
MOTOR CORTEX
Pathology
STRIATUM MOTOR CORTEX
PALLIDUM THALAMUS
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STAGES OF PARKINSON'S DISEASE

DOPAMINE (% control) 100 80 ADAPTIVE CAPACITY 60 40 20 DECOMPENSATION 0
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COMPENSATION -no symptoms MILD SYMPTOMS MARKED SYMPTOMS

Levodopa therapy
Main treatment is with L-DOPA Precursor for dopamine Sinemet is L-DOPA + carbidopa carbidopa 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
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Drugs used to treat Parkinsons Disease
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Appears
Later in Life Continuous Progressive Neurological Disease, thereby causing increasing disability of movement no cure
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Etiology
Cerebral
atherosclerosis Viral encephalitis Side effects of several antipsychotic drugs (i.e., phenothiazides, butyrophenones, reserpine)
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Environmental factors and neurotoxins

Pesticides,
herbicides, industrial chemicals - contain substances that inhibit complex I in the mitochondria
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In Terms of Etiology and Clinical Picture, Major Symptoms Involve:
Bradykinesia- Slowness in Initiation and Execution of Voluntary Movements Rigidity - Increase Muscle Tone and Increase Resistance to Movement (Arms and Legs Stiff) Tremor - Usually Tremor at Rest, When Person Sits, Arm Shakes, Tremor Stops When Person Attempts to Grab Something Postural Instability - abnormal fixation of posture (stoop when standing), equilibrium, and righting reflex Gait Disturbance - Shuffling Feet
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Usually Other Accompanied Autonomic Deficits Seen Later in Disease Process:

Orthostatic Hypotension Dementia Dystonia Ophthalmoplegia Affective Disorders
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Parkinson Disease Neurochemistry
Loss of Dopaminergic (DA) Cells Located in Basal Ganglia; most symptoms do not appear until striata DA levels decline by at least 70-80%.
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Imbalance
primarily between the excitatory neurotransmitter Acetylcholine and inhibitory neurotransmitter Dopamine in the Basal Ganglia
DA
ACh
The Dopaminergic Neurons in the Basal Ganglia Are mainly affected Acetylcholine within striatum is a tonically activated neuron It impinges on GABA Neuron by an Excitatory Action GABA Neuron Has an Inhibitory Action on the Substantia Nigra from Substantia Nigra, Has a Dopaminergic Feed Back Loop Back to Striatum Which Gets Loss Giving Signs and Symptoms of Parkinson Disease
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Basal Ganglia
The Basal Ganglia Consists of Five Large Subcortical Nuclei That Participate in Control of Movement:
Caudate Putamen Globus
Nucleus
Pallidus Subthalamic Nucleus Substantia Nigra
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The balance of the five large Subcortical Nuclei are responsible for smooth motor movements
The primary input is from the Cerebral Cortex, and the output Is directed through the thalamus back to the Prefrontal, Premotor, and Motor Cortex The motor function of the basal ganglia are therefore mediated by the Frontal Cortex Neurotransmitters in Basal Ganglia Include Serotonin, Acetylcholine, GABA, Enkephalin, Substance P, Glutamate, and Dopamine Dopamine from Substantia Nigra decreases release of acetylcholine from striatum.
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Drug Therapy
Drug Therapy Against Parkinson Disease Is Aimed at Bringing the Basal Ganglia Back to Balance

Decrease Cholinergic Activity Within Basal Ganglia and this Can Be Done Two Ways: Activating Dopamine receptors in Substantia Nigra feeding back to Cholinergic Cells in the striatum Turn off the Cholinergic Cells, Then Things Are Brought Back to Balance Antagonize Acetylcholine receptors
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Agents that Increase Dopamine functions

Increasing the synthesis of dopamine - lDopa Inhibiting the catabolism of dopamine selegiline Stimulating the release of dopamine amphetamine Stimulating the dopamine receptor sites directly - bromocriptine & pramipexole Blocking the uptake and enhancing the release of dopamine - amantadine
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Dopamine and Tyrosine Are Not Used for Parkinson Disease Therapy
Dopamine Doesn't Cross the Blood Brain Barrier Huge amount of tyrosine decreases activity of rate limiting enzyme Tyrosine Hydroxylase That normally Converts Tyrosine to dopamine by overwhelming enzyme tyrosine hydroxylase, has a feedback loop that will turn off tyrosine hydroxylase
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L Dopa Therapy for Parkinson Disease

Dopamine
Decarboxylase Converts L Dopa to Dopamine That Gets Stored into Secretory Vesicles and Gets Released from Basal Ganglia
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Effects of L Dopa on the Symptoms of Parkinson Disease
L Dopa Fairly Effective in Eliminating Most of the Symptoms of Parkinson Disease Bradykinesia and Rigidity Quickly Respond to L Dopa Reduction in Tremor Effect with Continued Therapy L Dopa less Effective in Eliminating Postural Instability and Shuffling Gait Meaning Other Neurotransmitters Are Involved in Parkinson Disease
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Long Term Therapy

Behavioral Disturbances in 20 to 25% of Population Trouble in Thinking (Cognitive Effects) L Dopa Can Induce: Psychosis Confusion Hallucination Anxiety Delusion Some Individuals develop Hypomania Which Is Inappropriate Sexual Behavior; "Dirty Old Man", "Flashers"
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"On/off" Effect
"On/off" Effect Is like a Light Switch ; Without Warning, All of a Sudden, Person Goes from Full Control to Complete Reversion Back to Bradykinesia, Tremor, Etc. Lasting from 30 Minutes 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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Treat by Giving Small Dose Regiments from 16 to 20 Hours "On/off" Effect May Be Due to Composite of Amino Acids That Use Same Dopamine Transportor across Gastric Mucosa causing extremely low levels of L Dopa in CNS thereby causing symptoms of Parkinson Disease to reappear. Changing diet (to low protein), may cause large conc of L Dopa in CNS Giving thus producing an 'off' Effect of Symptoms of Parkinson Disease
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Bromocriptine
For Treating Parkinson Disease ; an Ergotamine derivative, acts as a Dopamine Receptor Agonist the Drug Produces Little Response in Patients That Do Not React to Levodopa
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Pramipexole
Pramipexole
Pramipexole is a nonergot dopamine agonist with high relative in vitro specificity and full intrinsic activity at the D2 subfamily of dopamine receptors, binding with higher affinity to D3 than to D2 or D4 receptor subtypes. Precise mechanism of action is unknown, although it is believed to be related to its ability to stimulate dopamine receptors in the striatum.
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Amantadine
Amantadine for Treating Parkinson Disease Amantadine Effective as in the Treatment of Influenza, however has significant Antiparkinson Action; it appears to Enhance Synthesis, Release, or Reuptake of Dopamine from the Surviving Nigral Neurons
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Deprenyl ( Selegiline)
Deprenyl ( Selegiline) for Treating Parkinson Disease Deprenyl Selectively Inhibits Monoamine Oxidase B Which Metabolizes Dopamine, but Does Not Inhibit Monoamine Oxidase a Which Metabolizes Norepinephrine and Serotonin
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The Protective Effects of Selegiline

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 the surviving striatal dopamine neurons accelerate the synthesis of dopamine, thus enhancing the formation of H202 according to the following scheme.
Amphetamine for Treating Parkinson Disease
Amphetamine Has Been Used Adjunctively in the Treatment of Some Parkinsonian Patients it Is Thought That, by Releasing Dopamine and Norepinephrine from Storage Granules, Amphetamine Makes Patients More Mobile and More Motivated
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Catechol-O-methyltransferase (COMT) inhibitors

Tolcapone (Tasmar) and Entacapone (Comtan) are two 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%
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Antimuscarinic Agents for Treating Parkinson Disease
The Antimuscarinic Agents Are Much less Efficacious than Levodopa, and These Drugs Play Only an Adjuvant Role in Antiparkinson Therapy the Actions of Atropine, Scopolamine, Benztropine, Trihexyphenidyl, and Biperiden Are Similar
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On the Horizon
A number of potential Parkinson's treatments in research laboratories now show much promise. They include:
Neurotrophic proteins--These appear to protect nerve cells from the premature death that prompts Parkinson's. One hurdle is getting the proteins past the blood-brain barrier. Neuroprotective agents--Researchers are examining naturally occurring enzymes that appear to deactivate "free radicals," chemicals some scientists think may be linked to the damage done to nerve cells in Parkinson's and other neurological disorders.
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Spinal Cord Spinal Cord
Tracts Tracts
Ascending Tracts Ascending Tracts

Posterior White Column-Medial Lemniscal Pathway Posterior White Column-Medial Lemniscal Pathway Spinothalamic Tract Spinothalamic Tract Spinoreticular or Spinoreticulothalamic Tract Spinoreticular or Spinoreticulothalamic Tract Spinocerebellar Tract Spinocerebellar Tract Spinomedullothalamic Tract Spinomedullothalamic Tract Cervicothalamic or Spinocervicothalamic Tract Cervicothalamic or Spinocervicothalamic Tract Spino-olivary Tract Spino-olivary Tract Spinotectal Tract Spinotectal Tract
Descending Tracts Descending Tracts
Descending Tracts from Brain Stem Descending Tracts from Brain Stem
Dorsolateral (Motor) Pathway Dorsolateral (Motor) Pathway Rubrospinal Tract Rubrospinal Tract Ventromedial (Motor) Pathway Ventromedial (Motor) Pathway Tectospinal Tract Tectospinal Tract Vestibulospinal Tract Vestibulospinal Tract MLF (Medial Longitudinal Fasciculus) MLF (Medial Longitudinal Fasciculus) --interstitiospinal tract interstitiospinal tract Sensory Modulation pathways Sensory Modulation pathways Raphespinal & Cerulospinal Pathways Raphespinal & Cerulospinal Pathways Descending Autonomic Pathways Descending Autonomic Pathways
Upper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) Syndrome UMN syndrome Type of Paralysis Atrophy Deep Tendon Reflex Pathological Reflex Superficial Reflex Fasciculation and Fibrillation
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LMN Syndrome Flaccid Paralysis Severe Atrophy Absent DTR Absent Present Could be Present
Spastic Paresis No (Disuse) Atrophy Increase Positive Babinski Sign Absent Absent
Syndrome Syndrome
Predominantly Motor Syndromes Poliomyelitis (Infantile Paralysis)

- viral infection of lower motor neuron - LMN syndrome at the level of lesion
Amyotrophic Lateral Sclerosis (ALS)

- combined LMN and UMN lesion - LMN syndrome at the level of lesion - UMN syndrome below the level of lesion - Lou Gehrigs disease
Syndrome Syndrome
Predominantly Sensory Syndromes Herpes Zoster

- inflammatory reactions of spinal ganglion - severe pain on the dermatomes of affected ganglion
Tabes Dorsalis
- common variety of neurosyphilis - posterior column and spinal posterior root lesion - loss of discriminative touch sensation and conscious proprioception below the level of lesion - posterior column ataxia - lancinating pain (a stabbing or piercing sensation) - loss of deep tendon reflex (DTR)
Syndrome Syndrome
Sub-Acute Combined Degeneration (Combined System Disease)

Lesion - posterior white column - corticospinal tract (UMN) Symptom - loss of discriminative touch sensation and conscious proprioception below the level of lesion - ipsilateral UMN syndrome below the level of lesion
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Syndrome Syndrome
Syringomyelia, Hematomyelia
Lesion - central canal of spinal cord - gradually extended to peripheral part of the cord Symptom - initial symptom is bilateral loss of pain (compression of anterior white commissure) - variety of symptoms appear according to the lesion extended from central canal
Syndrome Syndrome
Brown-Sequard syndrome
(spinal cord hemisection)
Major Symptoms 1. ipsilateral UMN syndrome below the level of lesion 2. ipsilateral LMN syndrome at the level of lesion 3. ipsilateral loss of discriminative touch sensation and conscious proprioception below the level of lesion (posterior white column lesion) 4. contralateral loss of pain and temperature sensation below the level of lesion (spinothalamic tract lesion)
Interferon Beta 1a (Avonex and Rebif):

Is a protein that is a replica of human interferon. It suppress the immune system and helps to maintain the blood-brain barrier. You inject Avonex into the muscle once a week and Rebif is injected under the skin three times a week. This drug is useful to people who have definite progressive MS. One side effect of the drug is a flu like symptom.
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Courses of MS
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Relapse-remitting MS (RRMS):
Here have an attack, go into complete or partial remission, then have the symptoms return.
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Primary-progressive MS (PPMS):
Here continually decline and have no remissions. There may be a temporary relief in symptoms. A few patients have malignant MS which is where they have a quick decline which leaves them severely disabled or even lead to death.
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Secondary-progressive MS (SPMS):
This stage of MS starts with RRMS symptoms and continues on to show signs of PPMS.
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Progressive-relapsing MS (PRMS):
This is a rare form but here it takes a progressive route made worse by acute attacks. 20% of the people with MS have a benign form. Here they show little progression after the first attack.
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CNS EXAMINATION

HIF CRANIAL NERVES MOTOR SYSTEM SENSORY SYSTEM CEREBALLAR SIGNS MENINGEAL SIGNS GAIT
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LMN LESION;

WEAKNESS HYPOTONIA AREFLEXIA WASTING DISTRIBUTION OF WASTING / WEAKNESS CONSISTENT WITH LESION IN NERVE SEGMENT, NERVE ROOT & PERIPHERAL NERVE.
11/07/11
UMN LESION
WEAKNESS IN CORTICOSPINAL DISTRIBUTION, SH.AB, HIP.FLEX & DORSIFLEXION FINE & DISTAL MOVEMENTS EPR SPASTICITY HYPERREFLEXIA LITTLE OR NO ATROPHY
11/07/11
EPD / DYSTONIA
PLASTIC OR SPASTIC INCREASE IN MUSCLE TONE ABNORMAL POSTURES INVOLUNTARY MOVEMENTS & TREMORS NORMAL OR INCREASED REFLEXES PLANTAR RESPONSES NORMAL OR EXTENSOR
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EPS

BASAL GANGLIA (CLASS), STUCTURES IN THE BRAIN STEM NO DIRECT PATHWAYS FROM BASAL GANGLIA TO THE SPINAL CORD. FIBRES FROM CEREBRAL CORTEX & THALAMUS DENTATORUBRO SPINAL, RETICULO SPINAL, VESTIBULOSPINAL & OLIVOSPINAL. CONTROL OF POSTURE & IN THE INITIATION OF MOVEMENT
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EPS LESION
DIFFICULTY IN INITIATING VOLUNTARY MOVEMENT IMPAIRMENT OF ORIENTING & BALANCING REFLEXES. ALTERATION IN MUSCLE TONE STRENGTH IS UNAFFECTED. INVOLUNTARY MOVEMENTS.
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CEREBELLUM
RECEIVES AFFERENT FIBRES FROM SPINAL CORD, VESTIBULAR SYSTEM, BASAL GANGLIA & CEREBRAL CORTEX. MODULATE MOVEMENT
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CEREBELLAR LESION

ATAXIA VERMIS; TRUNCAL ATAXIA (DIFFICULTY IN SITTING UP OR STANDING) REFLEXES ARE NOT INCREASED.
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INTRINSIC CORD LESION

URGE INCONTINENCE /R.O.U DISSOCIATED SENSORY LOSS SPINOTHALAMIC PAIN BILATERAL CORTICOSPINAL TRACT SIGNS PARAPLEGIA & SENSORY LEVEL
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SPEECH DEFINITIONS
APHASIA; DISORDER OF LANGUAGE CONTENT OF SPEECH ANOMIA; INABILITY PRODUCE CORRECT WORD PARAPHASIA; PRODUCE NONSENSE WORD
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BROCAS APHASIA

MOTOR APHASIA (unable to express) EXPRESSIVE APHASIA NON-FLUENT GOOD COMPREHENSION POOR REPETITION INFERIOR FRONTAL GYRUS LESION LESIONS ANTERIOR TO THE CENTRAL FISSURE
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WERNICKES APHASIA

SENSORY RECEPTIVE LOST FLUENT (SPEAK WITHOUT MEANING) POOR COMPREHENSION POOR REPETITION LESIONS POSTERIOR TO THE CENTRAL FISSURE
11/07/11
BRAIN-STEM SYNDROMES
WEBER (ANTERIOR CEREBRAL PEDUNCLE MIDBRAIN) IL3+CL7UMN+CLHP CLAUDE; CEREBRAL PEDUNCLE INVOLVING RED NUCLEUS IL3 + CL CEREBELLAR SIGNS
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PARINAUD;

DORSAL MB/ TECTUM VERTICAL GAZE PALSY+ CONVERGENCE DISORDERS + CONVERGENCE RETRACTION+ NYSTAGMUS+ PUPILLARY & LID DISORDERS
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MILLARD-GUBLAR;

PONTO-MEDULLARY Jn. IL6+IL7LMN CLHP
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WALLENBERG;LATERAL MEDULLARY SYNDROME;
IL5,9,10,11+IL HONER+IL CEREBELLAR+ CL SPINOTHALAMIC VESTIBULAR DISTURBANCE.
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DEFINITIONS
CONSCIOUSNESS; IS A STATE OF AWARENESS ONES SELF & ONES ENVIRONMENT SLEEP; IS A STATE OF PHYSICAL & MENTAL INACTIVITY FROM WHICH THE PT. CAN BE AROUSED TO NORMAL CONSCIOUS
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DROWSINESS
IS A PATHOLOGICAL STATE THAT RESEMBLES NORMAL SLEEP. PT. CAN BE AROUSED WITH AN EXTERNAL STIMULUS, BUT REVERTS BACK TO HIS DROWSY STATE ON WITHDRAWAL OF STIMULUS
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COMA & SEMICOMA

IS THE DEEPEST LEVEL OF UNC. PT. IS IMMOBILE , ALL THE REFLEXES ARE ABSENT AND PLANTAR IS EXTENSOR. SEMICOMA; IS A PATHOLOGICAL STATE, WHICH REQUIRES STRONGER STIMULUS TO AROUSE THE PT., THOUGH HIS REFLEXES ARE NORMAL.
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INVOLUNTARY MOVEMENTS
TREMOR; REGULAR & RHYTHMIC OSCILLATORY MOVEMENTS OF AGONIST & ANTAGONIST MUSCLES CHOREA; QUICK, BREIF, SUDDEN, JERKY & IRREGULAR IN TIME, RHYTHM, CHARACTER & PLACE OF OCCRRENCE PROXIMALLY UNDER COVER OF HYPOTONIA
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ATHETOSIS; SLOW RHYTHMIC, WRITHING MOVEMENTS DISTALLY & HYPERTONIC. HEMIBALLISMUS; UL, RAPID, CONTINUOUS, INVOLUNTARY MOVEMENTS WITH WIDE EXCURSIONS AFFECTING THE PROXIMAL PARTS OF BODY
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DYSTONIA; IT IS AN ABNORMALLY INCREASED MUSCLE TONE THAT CAUSES FIXED ABNORMAL POSTURES OR SHIFTING POSTURES RESULTING FROM IRREGULAR, FORCEFUL TWISTING MOVEMENTS THAT AFFECT THE TRUNK & LIMBS.
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FASCICULATIONS; VISIBLE TWITCHES OF HYPEREXCITED MUSCLE FIBRES. IRREGULAR & INCONSISTENT. ABSENT AT REST, FIBRILLATION; CONTRACTION LIMITED TO A SINGLE MUSCLE FIBRE OR A SMALL GROUP OF MUSCLE FIBRES. PRESENT ON TONGUE. SMA, MND, DM, SYPHILIS, SYRINGOMYELIA
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TICS OR HABIT SPASMS
INVOLUNTARY STEREOTYPED MOVEMENTS WHICH TO START WITH ARE VOLUNTARY AS THEY SERVE SOME PURPOSE, BUT LATER PERSIST EVENTHOUGH THE STIMULUS THAT INITIATED THE MOVEMENT HAS CEASED.
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MYOKIMIA

TRANSIENT OR PERSISTENT QUIVERING FLICKERING MOVEMENTS WHICH AFFECT A FEW MUSCLE BUNDLES WITH IN A SINGLE MUSCLE USUALLY ARE NOT EXTENSIVE ENOUGH TO CAUSE A MOVEMENT.
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MYOCLONUS
MYOCLONUS; BRIEF SHOCK-LIKE

MUSCULAR CONTRACTION, WHICH INVOLVE THE WHOLE MUSCLE OR SMALL NUMBER OF MUSCLE FIBRES. IT IS DECREASED BY VOLUNTARY RELAXATION BRIEF, ISOLATED, RANDOM & NONPURPOSEFUL JERKS OF MUSCLE GROUPS IN THE LIMBS.
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ASTEREXIS OR FLAPPING TREMOR

INTERMITTENT FAILURE OF PARIETAL MECHANISMS. PT. IS ASKED TO HOLD OUT THE ARMS WITH THE HANDS EXTENDED AT THE WRISTS, THIS POSTURE IS PERIODICALLY DROPPED, ALLOWING THE HANDS TO DROP TRANSIENTLY BEFORE THE POSTURE IS TAKE IT AGAIN.
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LMN BLADDER (ATONIC)

S234 LESION LESION OF SACRAL ROOTS & NERVES LOSS OF DETRUSOR CONTRACTION DIFFICULTY INITIATING MICTURITION BLADDER DISTENTION WITH OVERFLOW
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HYPERTONIC (UMN)

PYRAMIDAL TACT LESION SPINAL CORD / BRAINSTEM URGENCY / URGE INCONTINENCE BLADDER SPHINCTER INCOORDINATION (DYSSYNERGIA) INCOMPLETE BLADDER EMPTYING
11/07/11
GCS 15 EMV

EYE OPENING; SPONTANEOUS, TO SPEECH, TO PAIN & NIL (4) MOTOR RESPONSE; OBEYS, LOCALIZED, WITHDRAWS, ABNORMAL FLEXION, EXTENSOR RESPONSE & NIL (6) VERBAL RESPONSE; ORIENTED, CONFUSED CONVERSATION, INAPPROPRIATE WORDS, INCOMPREHENSIBLE SOUNDS & NIL (5)
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EXTRINSIC CORD LESIONS
ROOT PAIN, WORSENED BY MOVEMENT PROGRESSIVE ASYMMETRICAL PARAPARESIS BSS PARAPLEGIA WITH SENSORY LEVEL INCONTINENCE / RETENSION OF URINE & FAECES
11/07/11
SENSORY DERMATOME ANTERIOR ASPECT

VERTEX; C1 PINNA; C2 NECK; C3 SHOULDER; C4 ARM LATERAL ; C5 MIDDLE ; T1 MEDIAL ; T2 FOREARM LATERAL; C6 MEDIAL ; C8 MIDDLE FINGER ; C7
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SENSORY DERMATOME

HAND ; C678 VERTEX / NECK / AXILLA ; C234 ARM / FA POST LATERAL; C5 INNER AXILLARY FOLD; D3 FA POST MEDIAL; D1
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SOLE OF FOOT

S1 BULK L5 GREAT TOE REVERSE IN DORSUM OF FOOT L5 BULK S1 LITTLE TOE
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ANTERIOR LEG

L2 UPPER THIGH L3 LOWER THIGH L4 UPPER LEG L5 LOWER LEG & FOOT L2,3,4 Knee Jerk
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POSTERIOR LEG

S2,3,4 saddle shaped L1,2,3 lateral aspect thigh
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Spinal segment related to vertebral body

Cervical vertebrae Thoracic 1 6 Thoracic 7 9 Thoracic 10 Thoracic 11 Thoracic 12 First lumbar arch
: add 1 : add 2 : add 3 : L1 & L2 : L3 & L4 : L5 : sacral & coccygeal segments
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Sensory polyneuropathy

Glove and stocking anesthesia Distal parts All modalities lost
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Cauda equina and conus lesion

Perianal anesthesia S234 involvement
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Brown Sequerd syndrome

Hemi section of cord lesion Ipsi lateral loss pyramidal and posterior columns signs Contra lateral spino thalamic tract signs Band of hyperesthesia
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High cord compression

Sacral sparing Loss of all modalities of sensations
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Dissociate anesthesia

Central cord lesion Sparing posterior columns Involvement of spino thalamic tracts Syringomyelia & Ketamine
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Brain stem syndrome
Loss of spino thalamic tract signs on IPSILATERAL side of face Loss of spino thalamic tract signs on CONTRA LATERAL side of body Involvement of Trigeminal tract or nucleus & lateral spinothalamic tracts.
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Thalamic syndrome
Loss of all modalities of sensations on opposite side of the body. Position sense is more affected than any other sensation. There may be spontaneous pain and discomfort (thalamic pain) Torturing and disabling type.
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Parietal lobe syndrome

Loss of tactile localization Loss of tactile discrimination Tactile extinction Astereognosis
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Anterior spinal syndrome
Anterior spinal artery thrombosis Loss of spino thalamic signs on both sides Preservation of posterior columns
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Posterior spinal syndrome

Posterior spinal artery thrombosis Loss of posterior columns on both sides Preservation of spino thalamic signs Noticed in Tabes dorsalis
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Common Causes Thrombosis
Lacunar stroke (small vessel) Large vessel thrombosis Dehydration
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Embolic
occlusion
Artery-to-artery
Carotid bifurcation Aortic arch Arterial dissection
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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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Uncommon Causes
Hypercoagulable
disorders
Protein C deficiency Protein S deficiency Antithrombin III deficiency Antiphospholipid syndrome Factor V Leiden mutationa Prothrombin G20210 mutationa Systemic 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 sinous thrombosis Fibromuscular 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
Cardiogenic
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Risk Factors for Stroke

Risk Factor Relative Risk Relative Risk Reduction with Treatment Primary Prevention Secondary Prevention Hypertension 2538%10030050100 Atrial fibrillation 1.82.968%warfarin, 21% aspirin 208313 Diabetes1.86No proven effect Smoking1.850% at 1 year, baseline risk at 5 years post cessation Hyperlipidemia1.82.61630%560230 Asymptomatic carotid stenosis2.053%85N/ Asymptomatic carotid stenosis (7099%) 65% at 2 yearsN/A12 Symptomatic carotid stenosis (5069%) 29% at 5 yearsN/A77
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Definition of Stroke: 11/07/11 MUN FP Academic Half Day 1

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Definition Of Stroke

MUN FP Academic Half Day

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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

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Causes of Ischemic Stroke

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Subarachnoid hemorrhage vasospasm Drugs: cocaine, amphetamine Moyamoya disease Eclampsia

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Fibro muscular dysplasia

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"Puff of smoke" (moyamoya in Japanese)

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Bleeding or other symptoms

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Large AVMs of the anterior circulation

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Superior pontine syndrome

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Middle pontine syndrome

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Inferior pontine syndrome

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Lateral midbrain syndrome

MUN FP Academic Half Day

IPSILATERAL (medial syndromes)

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IPSILATERAL (medial syndromes)

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IPSILATERAL (medial syndromes)

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IPSILATERAL (medial syndromes)

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