Neurology High Yield ( http://www.neuroanatomy.ca/module_list.html )
Ischemic Brain Disease
IRREVERSIBLE DAMAGE after 5 minutes
Most vulnerable Hippocampus pyramidal, cerebellum purkinjie cells,
watershed areas
Risks: diabetes, smoking, ATRIAL FIBRILLATION, cocaine
Transient attack: less than 24 hours neurological deficit
Types or stroke
1. Thrombotic/atherosclerotic: MOST COMMON
-pale liquifactive necrosis (NO REFERFUSION)
-causes reactive Gliosis cystic cavity
-usually MCA therefore at periphery
2. Embolic
-Hemorrhagic red infarct (DUE TO REPERFUSION)
-usually atrial fibrillation or atherosclerotic plaques
-MCA
3. Lacunar Infarct
-small perforating vessels (at BASAL GANGLIA ) hyaline
arteriosclerosis
-Causes: diabetes, HTN
4. Hemorrhagic stroke
-from aneurysm
-CharcotBouchard microaneursym at basal ganglia
of lenticulostriate arteries
-from reperfusion of ischemic
5. Watershed Infarct
-prolonged HYPOTENSION
-damage usually bilateral deep cortical areas btw border of two
vessels
-ACA- MCA Top
-MCA- PCA Bottom
Ischemic stroke Hemorrhagic stroke
Diminished blood flow Hemorrhage aneurysm
Leads to Gliosis Embolic
Watershed infarct Reperfusion
Artery Deficient
MCA -Aphasia (Wernicke or brocas),
-Neglect syndrome (if right parietal, so ignore left side)
-hemiparesis weakness ( arm and face)
-homonymous hemianopsia (temporal more common, so superior
quadrant)
ACA -LEG paresis
-hemiplegia (total paralysis)
, urinary incontinence
PCA -homonymous hemianopsia with macular sparing (since MCA give
blood)
Basilar Affect pons ( cranial nerves, coma, apnea, vertigo)
Lacunar -Pure motor ( internal capsule)
stroke -Pure sensory (thalamus) but the smell intact (since only sensory
that bypass)
-dysarthria
-Ataxic hemiparesis (ipsilateral clumpsy
Imaging:
ACUTE do CT to see if hemorrhagic (dark on CT after 24 hours)
MRI shows up bright in 3-30 min and remain bright 10 days
Histology
12-24 H : RED neurons
24-72: necrosis + PMN
3 -5 day : macrophage
1-2 week : reactive gliosis + vascular proliferation
>2 week: glial scar
Treatment
tPA for occlusive (give within 3 hours)
warfarin/ aspirin for embolic once hemorrhage has been ruled out
Alzheimers
Diffuse cortical atrophy (widen sulci, narrow gyri, expand ventricles, ex
vacuo hydrocephalus )
Nucleus basalis of Meynert ( low ACH)
MOST COMMON cause of dementia ( 2nd is stroke)
Causes
1. Apolipoprotein E 2protective ( “ 2 serve and protect”)
2. ‘’ E4 increases risk
3. Down Syndrome, chromosome 21 has APP (amyloid precursor
protein) * will stain with Congo red
-usually get it before 40
4. Presenilin
-Presenilin 1 (chromosome 14)
-‘’ 2 (chromosome 1)
Clinical diagnosis (confirmed on autopsy)
Histology
Senile/ neuritic plaques : ABETA-amyloid (beta cleavage of APP)
EXTRACELLULAR
-normal cleavage if ALPHA
Neurofibrillary tangles INTRACELLULAR in neurons
-HYPER phosphorylated Tau proteins which are microtubule
associated
, -amount of tangles CORRELATED WITH DEGREE OF
DEMENTIA
Death: infection, penumonia
Diseases of myelination
Guillain- Barre Syndrome/ Acute inflammation Demylinating
polyradiculopathy (PNS and motor + autonomic)
Endoneurium and Schwann cells attacked = autoimmune demyliantion
1-3 weeks post GI infection OR RESPIRATORY (campylobacter jejuni) or
herpes
SYMMETRIC Ascending paralysis MOTOR AND AUTONOMIC
Physical exam:
Decrease or absent reflex
Facial paralysis if ascended to face
Autonomic dysfunction : cardiac and blood pressure fluctuation
Need to give respiratory support
Lumbar puncture: high protein, normal cell count (albuminocytologic
dissociation)
-this high protein is also seen in intracranial cancer
Progressive Multifocal Leukoencephalopathy( PML) (CNS )
Demylination by destruction of oligodendrocytes
Associated with JC virus reactivation in AIDS patients (polyomavirus,ds
DNA)
Dementia and neurological deficits with RAPID PROGRESSION
Typically fatal
Histology: widespread demylination, astrogliosis, lymphohistiocytosis
* associated with Natalizumab ( drug against alpha-integrin used in Crohns
and MS) *MS also demylination oligodendrocytes
Usually seen on one side more
Ischemic Brain Disease
IRREVERSIBLE DAMAGE after 5 minutes
Most vulnerable Hippocampus pyramidal, cerebellum purkinjie cells,
watershed areas
Risks: diabetes, smoking, ATRIAL FIBRILLATION, cocaine
Transient attack: less than 24 hours neurological deficit
Types or stroke
1. Thrombotic/atherosclerotic: MOST COMMON
-pale liquifactive necrosis (NO REFERFUSION)
-causes reactive Gliosis cystic cavity
-usually MCA therefore at periphery
2. Embolic
-Hemorrhagic red infarct (DUE TO REPERFUSION)
-usually atrial fibrillation or atherosclerotic plaques
-MCA
3. Lacunar Infarct
-small perforating vessels (at BASAL GANGLIA ) hyaline
arteriosclerosis
-Causes: diabetes, HTN
4. Hemorrhagic stroke
-from aneurysm
-CharcotBouchard microaneursym at basal ganglia
of lenticulostriate arteries
-from reperfusion of ischemic
5. Watershed Infarct
-prolonged HYPOTENSION
-damage usually bilateral deep cortical areas btw border of two
vessels
-ACA- MCA Top
-MCA- PCA Bottom
Ischemic stroke Hemorrhagic stroke
Diminished blood flow Hemorrhage aneurysm
Leads to Gliosis Embolic
Watershed infarct Reperfusion
Artery Deficient
MCA -Aphasia (Wernicke or brocas),
-Neglect syndrome (if right parietal, so ignore left side)
-hemiparesis weakness ( arm and face)
-homonymous hemianopsia (temporal more common, so superior
quadrant)
ACA -LEG paresis
-hemiplegia (total paralysis)
, urinary incontinence
PCA -homonymous hemianopsia with macular sparing (since MCA give
blood)
Basilar Affect pons ( cranial nerves, coma, apnea, vertigo)
Lacunar -Pure motor ( internal capsule)
stroke -Pure sensory (thalamus) but the smell intact (since only sensory
that bypass)
-dysarthria
-Ataxic hemiparesis (ipsilateral clumpsy
Imaging:
ACUTE do CT to see if hemorrhagic (dark on CT after 24 hours)
MRI shows up bright in 3-30 min and remain bright 10 days
Histology
12-24 H : RED neurons
24-72: necrosis + PMN
3 -5 day : macrophage
1-2 week : reactive gliosis + vascular proliferation
>2 week: glial scar
Treatment
tPA for occlusive (give within 3 hours)
warfarin/ aspirin for embolic once hemorrhage has been ruled out
Alzheimers
Diffuse cortical atrophy (widen sulci, narrow gyri, expand ventricles, ex
vacuo hydrocephalus )
Nucleus basalis of Meynert ( low ACH)
MOST COMMON cause of dementia ( 2nd is stroke)
Causes
1. Apolipoprotein E 2protective ( “ 2 serve and protect”)
2. ‘’ E4 increases risk
3. Down Syndrome, chromosome 21 has APP (amyloid precursor
protein) * will stain with Congo red
-usually get it before 40
4. Presenilin
-Presenilin 1 (chromosome 14)
-‘’ 2 (chromosome 1)
Clinical diagnosis (confirmed on autopsy)
Histology
Senile/ neuritic plaques : ABETA-amyloid (beta cleavage of APP)
EXTRACELLULAR
-normal cleavage if ALPHA
Neurofibrillary tangles INTRACELLULAR in neurons
-HYPER phosphorylated Tau proteins which are microtubule
associated
, -amount of tangles CORRELATED WITH DEGREE OF
DEMENTIA
Death: infection, penumonia
Diseases of myelination
Guillain- Barre Syndrome/ Acute inflammation Demylinating
polyradiculopathy (PNS and motor + autonomic)
Endoneurium and Schwann cells attacked = autoimmune demyliantion
1-3 weeks post GI infection OR RESPIRATORY (campylobacter jejuni) or
herpes
SYMMETRIC Ascending paralysis MOTOR AND AUTONOMIC
Physical exam:
Decrease or absent reflex
Facial paralysis if ascended to face
Autonomic dysfunction : cardiac and blood pressure fluctuation
Need to give respiratory support
Lumbar puncture: high protein, normal cell count (albuminocytologic
dissociation)
-this high protein is also seen in intracranial cancer
Progressive Multifocal Leukoencephalopathy( PML) (CNS )
Demylination by destruction of oligodendrocytes
Associated with JC virus reactivation in AIDS patients (polyomavirus,ds
DNA)
Dementia and neurological deficits with RAPID PROGRESSION
Typically fatal
Histology: widespread demylination, astrogliosis, lymphohistiocytosis
* associated with Natalizumab ( drug against alpha-integrin used in Crohns
and MS) *MS also demylination oligodendrocytes
Usually seen on one side more