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Neuro Flashcards

1
Q

What are the two major functional elements of peripheral nerves?

A
  1. Axonal processes

2. myelin sheaths

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2
Q

Describe morphological changes associated with axonal degeneration

A

Axonal neuropathies are caused by direct injury to the axons themselves. Degeneration of axon distal to the injury. Decreased axon density, causes decrease in strength/amplitude of nerve impulses.

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3
Q

Describe morphological changes associated with demyelination.

A

Damage to Schwann cells/myelin resulting in slow nerve conduction. No change in density of axons. Areas of demyelination may have repairs underway.

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4
Q

Describe polyneuropathies

A
  1. Usually affect peripheral nerves in a symmetric, length dependent fashion.
  2. Axonal loss is typically more pronounced in the distal segments of longest nerves.
  3. Loss of sensation and paresthesia starts in toes and spreads upwards.
  4. “stocking-and-glove distribution” by the time sensory changes reach level of knees, hands are also affected.
  5. Associated with toxic and metabolic damage.
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5
Q

Describe mononeuritis multiplex

A
  1. Damage randomly affects individual nerves (e.g. right radial nerve palsy and wrist drop, and later left foot drop)
  2. Often caused by vasculitis.
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6
Q

Describe simple mononeuropathy

A

Most commonly result of traumatic injury, or infections such as lyme disease

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7
Q

Define Guillain-Barre syndrome

A
  1. Rapidly progressive acute demylinating disorder affecting motor axons, resulting in ascending weakness.
  2. Inflammatory peripheral neuropathy.
  3. Can cause death from failure of respiratory muscles.
  4. Triggered by vaccination or infection (EBV, Zika, Campylobacter jejuni)
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8
Q

Define myasthenia gravis

A
  1. Autoimmune disease with fluctuating muscle weakness that is caused by antibodies that target the nueromuscular junction.
  2. Antibodies block, alter, or destroy postsynaptic Acetycholine receptor.
  3. S/S include can include ptosis and diplopia
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9
Q

What is cerebral edema?

A

Accumulation of excess fluid within the brain.

  1. Vasogenic: disruption in blood-brain-barrier, fluid shifts from vascular compartment to extracellular spaces.
  2. Cytotoxic: Increase in intracellular fluid due to neuronal and glial cell injury
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10
Q

What is hydrocephalus?

A

Increase in CSF volume in ventricular system due to impaired flow or decreased reabsorption.

  1. Communicating: entire ventricular system is involved.
  2. Noncommunicating: localized obstacle to CSF flow, only portion of ventricles enlarged.
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11
Q

What is brain herniation?

A

Displacement of brain tissue from one compartment to another in response to increased intracranial pressure.

  1. Subfalcine (cingulate): unilateral or asymmetric expansion of cerebral hemisphere displaces cingulate gyrus.
  2. Transtentorial (cingulate): medial aspect of temporal lobe is compressed against free margin of tentorium.
  3. Tonsillar herniation: Displacement of cerebellar tonsils through foramen magnum, causes brain stem compression that can be fatal.
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12
Q

Describe two mechanisms by which the brain may be deprived of oxygen.

A
  1. Functional hypoxia: low partial pressure of oxygen, impaired oxygen-carrying capacity, or toxin interfering with oxygen use.
  2. Ischemia: secondary to hypoperfusion, caused by hypotension, or vascular obstruction
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13
Q

Describe mechanism and clinical outcomes of global cerebral ischemia.

A
  1. Mechanism: generally occurs from drop of systolic pressure below 50 mm Hg.
  2. Clinical outcomes: mild (post-ischemic confusional state) or severe (brain death)
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14
Q

What is focal cerebral ischemia?

A

Cerebral arterial occlusion, first leads to focal ischemia and then to infarction in the distribution of compromised vessel.

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15
Q

Describe embolic infarctions.

A
  1. Cardiac mural thrombi are frequent source.
  2. Myocardial dysfunction, valvular disease, and a-fib are predisposing factors.
  3. Thromboemboli arise in arteries from atheromatous plaques in carotid arteries or aortic arch.
  4. Tend to lodge where vessels branch or in areas of stenosis (middle cerebral artery most common).
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16
Q

Describe thrombotic occlusions.

A
  1. Superimposed on atherosclerotic plaques.
  2. Common sites: carotid bifurcation, origin of middle cerebral artery, either end of basilar artery.
  3. Lacunar infarcts: small infarcts only a few millimeters caused by long-standing hypertension.
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17
Q

Describe nonhemorrhagic infarcts

A
  1. Result from acute vascular occlusions.

2. Tissue liquefies and leaves a fluid filled-cavity, gradually expands.

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18
Q

Describe Hemorrhagic infarcts

A
  1. Reperfusion of ischemic tissue through collaterals or after dissolution of emboli.
  2. Manifest as petechial hemorrhages.
19
Q

What are 3 main causes of intracranial hemorrhages?

A
  1. hypertension and diseases of vascular wall
  2. Structural lesions such as arteriovenous or cavernous malformations
  3. tumors
20
Q

What is Primary intraparenchymal hemorrhage?

A
  1. Rupture of small intraparenchymal vessel, underlying cause of hypertension or cerebral amyloid angiopathy.
  2. Extravenous blood compresses parenchyma, shows as cavity with brown rim
21
Q

What is Subarachnoid hemorrhage and saccular (berry) aneurysms?

A
  1. Rupture of a saccular aneurysm.
  2. Location: anterior circulation near major arterial branch points.
  3. Morphology: Thin walled outpouching of artery ruptures releasing blood into subarachnoid space, substance of brain, or both.
22
Q

What is arteriovenous malformation?

A
  1. Manifests with seizures, intracerebral hemorrhage or subarachnoid hemorrhage.
  2. Located in subarachnoid vessels extending into brain parenchyma or occur exclusively within hte brain.
  3. Tangled network of wormlike vascular channels.
23
Q

How is a contusion brain injury caused?

A

Caused by rapid tissue displacement, disruption of vascular channels, and subsequent hemorrhage, tissue injury, and edema.

24
Q

What is a concussion?

A

Describes reversible altered brain function, with or without loss of consciousness, from head injury.

25
Q

What is diffuse axonal injury?

A

More subtle widespread injury to axons within the brain, sometimes with devastating consequences.

26
Q

What is epidural hematoma?

A

Between dura and skull. Usually from skull fracture in children and adults (infants may form in absence of fracture). Blood accumulates under arterial pressure.
Patients may be lucid for several hours before neuro signs appear. Expands rapidly.

27
Q

What is a subdural hematoma?

A

Bleeding between two layers of the dura. Typically manifest within first 48 hours after injury. Slowly evolving neurological symptoms. Symptoms include headache and confusion.

28
Q

What are the 4 main routes of infectious spread in the nervous system.

A
  1. Hematogenous spread: travel via arterial blood supply, or retrograde venous spread (facial veins and venous sinus)
  2. Direct implantation: due to open/penetrating trauma or iatrogenic.
  3. Local extension: infections of skull or spine including: air sinuses, infected teeth, osteomyelitis, congenital malformation.
  4. Peripheral nerves: mainly viruses
29
Q

What is meningitis?

A

Inflammatory process involving the leptomininges (arachnoid and pia mater) within the subarachnoid space. If infection spreads into the underlying brain, it is meningoencephalitis.

30
Q

What are pathogens and signs/symptoms of pyogenic (bacterial) meningitis?

A
  1. E. coli, group B strep (infants), neisseria meningitis (young adults), strep. pneumoniae or listeria monocytogenes (older adults)
  2. S/S: systemic signs of infection, meningeal irritation, headache, photophobia, neck stiffness, “cloudy consciousness”
31
Q

What are pathogens and signs/symptoms of acute aseptic (viral) meningitis?

A
  1. Enteroviruses, measles, influenza species, lymphocytic choriomeningitis virus
  2. S/S: Less fulminant than pyogenic meningitis, lymphocytosis, moderate protein elevation, normal glucose levels. Bacteria can’t be cultured.
32
Q

What are pathogens and signs/symptoms of chronic meningitis?

A
  1. TB (mycobacterium tuberculosis), Spirochetal (borrelia burgdorferi, treponema pallidum), and Fungal (cryptococcus neoformans, histoplasma capsulatum, coccidioides immitis)
  2. S/S: TB (headache, malaise, mental confusion, vomiting, tuberculoma), Paretic neurosyphilis (insidious progressive loss of mental and physical functions, mood alterations, severe dementia), Tabes dorsalis (impaired proprioception and ataxia, loss of pain sensation)
33
Q

Describe differences between central and peripheral nervous system myelin.

A
  1. CNS: Oligodendrocyte processes myelinate >1 internode.

2. Schwann cells myelinate 1 internode

34
Q

Define multiple sclerosis

A

An autoimmune demyelinating disorder characterized by episodes of disease activity, separated in time, that produce white matter lesions that are separated in space.
Caused by environmental triggers, genetic predisposition, involves TH1 and TH17 T cells.

35
Q

What are symptoms of multiple sclerosis?

A

Gradual, often stepwise, accumulation of neurological deficits that occur from multiple relapses followed by episodes of remission, changes in cognitive function.

36
Q

Describe the neurological effects of thiamine deficiency.

A

Thiamine deficiency (beriberi). Particularly common with alcoholism.

  1. Wernicke encephalopathy syndrome: abrupt onset of confusion, abnormalities in eye movement, and ataxia.
  2. Korkasoff syndrome: irreversible profound memory disturbance.
37
Q

Describe alzheimer’s disease.

A
  1. Accumulation of AB plaques and tau tangles
  2. Most common cause of dementia in older adults
  3. Impaired higher intellectual function, memory impairment, altered mood and behavior.
38
Q

Describe frontotemporal lobar degeneration (FTLD), including Pick’s disease.

A

FTLD encompasses several disorders that preferentially affect frontal and temporal lobes. Distinguished by lesions including tau or TDP43. Progressive deterioration of language and changes in personality.
Pick disease associated with smooth, round inclusions called Pick bodies.

39
Q

Describe Parkinson’s disease.

A
  1. Hypokinetic movement disorder.
  2. Loss of dopaminergic neurons in substantia nigra
  3. Tremor, rigidity, bradykinesia, instability.
  4. Progresses over 10-15 years, producing severe motor slowing to point of immobility.
40
Q

Describe Huntington’s disease

A
  1. Autosomal dominant movement disorder.
  2. Associated with degeneration of striatum (caudate and putamen)
  3. Characterized by involuntary jerky movements of all parts of body, writhing movements of extremities.
  4. Progressive, death after disease course of 15 years.
41
Q

Describe Amytrophic lateral sclerosis (ALS)

A
  1. Results from death of lower motor neurons in spinal cord and brain stem, and upper motor neurons (Betz cells) in motor cortex.
  2. Lower moton neuron loss: denervation of muscles, muscular atrophy, weakness and fasciculations.
  3. Upper motor neuron loss: Paresis, hyperreflexia, spasticity, upward babinski, degeneration of corticospinal tracts.
  4. Sensation unaffected, may have cognitive impairment
42
Q

Describe unique characteristics of tumors in the nervous system

A
  1. Do not have morphologically evident premalignant or in situ stages
  2. Even low-grade lesions may infiltrate large regions of the brain, leading to serious clinical deficits, inability to be resected, poor prognosis.
  3. Anatomic site can influence outcome independent of histological classification (e.g. benign meningioma may cause cardiorespiratory arrest from compression of medulla)
  4. Even most highly malignant gliomas rarely spread outside CNS.
43
Q

List 5 most common primary sites of metastatic CNS lesions.

A
  1. Lungs
  2. Breast
  3. Skin (melanoma)
  4. Kidney
  5. GI tract

BCS (3 decks)

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