, Advanced Pathophysiology Exam 4
Neuro)
Lambert-Eaton Syndrome
A syndrome caused by autoantibodies that inhibit the function of presynaptic calcium channels,
leading to decreased release of acetylcholine into the synaptic cleft
Lambert-Eaton - Clinical Manifestations
*Strong link to lung cancer
*Muscle weakness that IMPROVES with repetitive stimulation
*Do not respond to cholinesterase inhibitors
Spinal cord trauma - patho
*Microscopic hemorrhages in central grey matter
*Axonal edema in white matter --> ischemia --> injury and degeneration
*Release inflammatory mediators -->necrosis and scar tissue formation
*Injury is maximal at injury site and two cord segments above and below it
Spinal cord trauma - Clinical manifestations
*Spinal shock (normal activity of the spinal cord stops at and below level of injury. Loss of spinal
reflexes.)
*Paraplegia, quadriplegia
*Autonomic dysreflexia
Brown-Sequard Syndrome
Occurs when there is trauma or lesion that affects one half of the spinal cord. Typically occurs in
the cervical region.
Brown-Sequard Syndrome - Clinical Manifestations
,*Loss of proprioception on the SAME side as the lesion
*Loss of voluntary motor function from the corticospinal tract on the SAME side as the lesion
*Loss of pain and temperature on the OPPOSITE side of the lesion
Syringomyelia
The presence of a cavity in the spinal cord. Usually caused by a tumor, cyst, or trauma.
Syringomyelia -Clinical Manifestations
Loss of pain and temperature sensation on both sides at the level of the lesion (Due to the
crossing of the lateral spinothalamic tract)
Stroke - Types
*Ischemic (embolic, thrombolic)
*Hemorrhagic
Atherosclerosis
Most common cause of thrombotic stroke
Internal carotid, middle cerebral, posterior cerebral, and basilar artery
Common sites of thrombotic stroke
Lacunar stroke
Microinfarcts that involve small cerebral arteries that penetrate the brainstem and thalamus.
May be clinically silent or produce motor and/or sensory deficits
Embolic stroke
Emboli traveling through the heart, aorta, and carotic arteries occlude the middle cerebral
artery.
Emboli traveling the vertebral and basilar arteries occlude the apex of the basilar artery
Ischemic stroke - pathogenesis
*Nerve cells within the ischemic focus are damaged and killed by energy deprivation
, *Neurons die at the edge of the ischemic region due to excessive stimulation of glutamate
receptors (neuronal excitotoxicity)
Neuronal excitotoxicity
*Depletion of ATP -->inhibits NA+K+ ATPase -->loss of normal ion gradient --> increased
extracellular glutamate levels
*Increased glutamate levels--> increased stimulation on postsynaptic cells --> influx of Ca+ into
neuronal cells --> cell death
**Glutamate receptor antagonists can be used to reduce size of ischemic lesions.
Hemorrhagic Stroke - Etiology
HTN, congenital ruptured aneurysm (most common), AV malformation, coag disorders, drug use
Hemorrhagic Stroke - Pathogenesis
*Intracranial hemorrhage --> increased ICP
*Cerebral edema, inflammation
*Ischemia/compression --> cell death
Hemorrhagic stroke - clinical manifestations
*Severe HA and sudden change in LOC
*Seizure
*Focal deficit dependent on location and extent of bleed
*Increased risk for re-bleed
Schizophrenia - Pathogenesis
*Genetic susceptibility + environment
*Structural abnormalities (enlarged later and 3rd ventricle; small thalamus, hippocampus,
temporal cortex, and amygdala)
*Biochemical (reduced activity in frontal cortex)
Neuro)
Lambert-Eaton Syndrome
A syndrome caused by autoantibodies that inhibit the function of presynaptic calcium channels,
leading to decreased release of acetylcholine into the synaptic cleft
Lambert-Eaton - Clinical Manifestations
*Strong link to lung cancer
*Muscle weakness that IMPROVES with repetitive stimulation
*Do not respond to cholinesterase inhibitors
Spinal cord trauma - patho
*Microscopic hemorrhages in central grey matter
*Axonal edema in white matter --> ischemia --> injury and degeneration
*Release inflammatory mediators -->necrosis and scar tissue formation
*Injury is maximal at injury site and two cord segments above and below it
Spinal cord trauma - Clinical manifestations
*Spinal shock (normal activity of the spinal cord stops at and below level of injury. Loss of spinal
reflexes.)
*Paraplegia, quadriplegia
*Autonomic dysreflexia
Brown-Sequard Syndrome
Occurs when there is trauma or lesion that affects one half of the spinal cord. Typically occurs in
the cervical region.
Brown-Sequard Syndrome - Clinical Manifestations
,*Loss of proprioception on the SAME side as the lesion
*Loss of voluntary motor function from the corticospinal tract on the SAME side as the lesion
*Loss of pain and temperature on the OPPOSITE side of the lesion
Syringomyelia
The presence of a cavity in the spinal cord. Usually caused by a tumor, cyst, or trauma.
Syringomyelia -Clinical Manifestations
Loss of pain and temperature sensation on both sides at the level of the lesion (Due to the
crossing of the lateral spinothalamic tract)
Stroke - Types
*Ischemic (embolic, thrombolic)
*Hemorrhagic
Atherosclerosis
Most common cause of thrombotic stroke
Internal carotid, middle cerebral, posterior cerebral, and basilar artery
Common sites of thrombotic stroke
Lacunar stroke
Microinfarcts that involve small cerebral arteries that penetrate the brainstem and thalamus.
May be clinically silent or produce motor and/or sensory deficits
Embolic stroke
Emboli traveling through the heart, aorta, and carotic arteries occlude the middle cerebral
artery.
Emboli traveling the vertebral and basilar arteries occlude the apex of the basilar artery
Ischemic stroke - pathogenesis
*Nerve cells within the ischemic focus are damaged and killed by energy deprivation
, *Neurons die at the edge of the ischemic region due to excessive stimulation of glutamate
receptors (neuronal excitotoxicity)
Neuronal excitotoxicity
*Depletion of ATP -->inhibits NA+K+ ATPase -->loss of normal ion gradient --> increased
extracellular glutamate levels
*Increased glutamate levels--> increased stimulation on postsynaptic cells --> influx of Ca+ into
neuronal cells --> cell death
**Glutamate receptor antagonists can be used to reduce size of ischemic lesions.
Hemorrhagic Stroke - Etiology
HTN, congenital ruptured aneurysm (most common), AV malformation, coag disorders, drug use
Hemorrhagic Stroke - Pathogenesis
*Intracranial hemorrhage --> increased ICP
*Cerebral edema, inflammation
*Ischemia/compression --> cell death
Hemorrhagic stroke - clinical manifestations
*Severe HA and sudden change in LOC
*Seizure
*Focal deficit dependent on location and extent of bleed
*Increased risk for re-bleed
Schizophrenia - Pathogenesis
*Genetic susceptibility + environment
*Structural abnormalities (enlarged later and 3rd ventricle; small thalamus, hippocampus,
temporal cortex, and amygdala)
*Biochemical (reduced activity in frontal cortex)
