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MW Flashcards

Patho, neuro

1
Q

Focal or diffuse injury to what specific region of the brain will result in a loss of consciousness or coma?

A

Diffuse injuries ( concussion or DIA) will typically cause an overall decreased level of consciousness. Whereas, focal injuries (such as an ICH or a contusion) will have symptoms based on the brain area affected

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2
Q

Define and compare focal and diffuse traumatic brain injury. What is the underlying structural and functional damage associated with diffuse brain injury?

A

The long connecting fibers in the brain called axons are sheared as the brain rapidly accelerates and decelerates inside the hard bone of the skull. DAI typically causes injury to many part of the brain, and people who suffer a DAI are usually left in a coma. The changes in the brain are often very tiny and can be difficult to detect using CT or MRI scans.

It is one of the most common types of traumatic brain injury and also one of the most devastating.

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3
Q

Kernig: what is it and how do you test for it?

A

A sign indicating the presence of meningitis (inflammation of the meninges covering the brain and spinal cord).
The test is done by having the person lie flat on the back, flex the thigh so that it is at a right angle to the trunk, and completely extend the leg at the knee joint.

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4
Q

Brudzinski’s sign:

A

is one of the physically demonstrable symptoms of meningitis. Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed.

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5
Q

How to test for Brudzinski?

A

Supine patient. Place one hand behind pt’s head, and another on their chest to prevent from rising. Then, lift patient’s head, bringing their chin to chest=involuntary flexing @ hip is a + sign

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6
Q

Parenchymal injury (TBI); skull fractures

A

all forms of TBI can involve both a primary (first injury) and secondary (brain swelling, release of intracellular ions/transmitters)

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7
Q

Focal brain injuries

A

Contusions, Lacerations

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8
Q

Diffuse Brain injury (diffuse axonal injury)

A

Concussion

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9
Q

Traumatic Vascular Injury

A

Hematomas:Epidural, Subdural, Subarachniod, and intraparenchymal

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10
Q

Mechanism of closed head injury

A

acceleration-head thrown forward while brain hits back of skull
deceleration-head thrown backwards while brain hits front of skull

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11
Q

Coup and contrecoup injuries

A

In head injury, a coup injury occurs under the site of impact with an object, and a contrecoup injury occurs on the side opposite the area that was hit. Coup and contrecoup injuries are associated with cerebral contusions, a type of traumatic brain injury in which the brain is bruised.

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12
Q

What type of injury causes Diffuse Brain Injury/Diffuse Axonal Injury?

A

Concussion

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13
Q

How many different grades of concussion?

A

Grade I and II - some disturbance in attention or memory but no loss of consciousness
Grade III - may involve brief loss of conscioussness (less than 5 minutes)
Grade IV – Classic Cerebral Concussion - an immediate loss in consciousness that lasts more than 5 minutes but less than 6 hours

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14
Q

What is considered a mild concussion?

A

Mild Concussion – temporary axonal disturbances

Grade I and II - some disturbance in attention or memory but no loss of consciousness

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15
Q

What might a grade III concussion involve?

A

Grade III - may involve brief loss of conscioussness (less than 5 minutes)

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16
Q

What is another name for Grade IV

A

Classic Cerebral Concussion - an immediate loss in consciousness that lasts more than 5 minutes but less than 6 hours

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17
Q

What does a Classic Cerebral Concussion involve?

A

Involves temporary disruption of the Reticular Activating System (RAS)

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18
Q

What is the RAS

A

The reticular activating system (RAS) is a network within the brainstem that plays a role in regulating the alertness, or arousal, of the brain and thus plays an important role in regulating wakefulness and sleep-wake transitions.

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19
Q

Acute Epidural Hematoma

A

occurs when a mass of blood forms in the space between the skull and the protective covering of the brain. … As it swells, the brain may shift in the skull. Pressure on and damage to the brain’s tissues can affect vision, speech, mobility, and consciousness.

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20
Q

Which artery is affected in an acute epidural hematoma?

A

The majority of bleeds originate from meningeal arteries, particularly in the temporal region. Middle meningeal artery-branches of middle meningeal artery

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21
Q

EDH or SEDH (spinal epidural hematoma)

A

An epidural hematoma (EDH) occurs when blood accumulates between the skull and the dura mater, the thick membrane covering the brain. They typically occur when a skull fracture tears an underlying blood vessel. EDHs are about half as common as a subdural hematomas and usually occur in young adults.

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22
Q

What does a Subdural Hematoma affect? (SDH)

A

Is a neurosurgical emergency!!! Is most often the result of a severe head injury. This type of hematoma is among the deadliest of all head injuries. The bleeding fills the brain area very rapidly, compressing brain tissue. This often results in brain injury and may lead to death.

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23
Q

Between what 2 membranes does a SDH occur?

A

A subdural hematoma (SDH) is a collection of blood below the inner layer of the dura but external to the brain and arachnoid membrane. Subdural hematoma is the most common type of traumatic intracranial mass lesion.

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24
Q

How are SDH characterized?

A

are usually characterized on the basis of their size and location and the amount of time elapsed since the inciting event age (ie, whether they are acute, subacute, or chronic)

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25
Q

What blood vessels are affected by SDH? Venous or arterial?

A

Typically, low-pressure venous bleeding from bridging veins dissects the arachnoid away from the dura, and the blood layers out along the cerebral convexity. Cerebral injury results from direct pressure, increased intracranial pressure (ICP), or associated intraparenchymal insults.Can be due to a ruptured small cortical artery but most often is due to rupture of bridging veins

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26
Q

Bridging veins that extend across to the superior aspect of the cerebral hemispheres are involved in what type of bleed?

A

SDH

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27
Q

What are the 4 types of CVAs?

A

Thrombotic Stroke
Embolic Stroke
Hemorrhagic Stroke
Lacunar Stroke

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28
Q

What is Global cerebral ischemia vs. Focal cerebral ischemia?

A

Lack of blood flow can affect the entire brain (global ischemia) or just a portion of it (focal ischemia). Ischemia can also be permanent, or transient if reperfusion occurs. This gives rise to a natural permutation of four general types of cerebral ischemia

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29
Q

What is the output hemisphere?

A

Motor cortex-left hemisphere section controls right side of body

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30
Q

What is the input area?

A

Sensory cortex-left hemisphere section receives input from body’s right side

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31
Q

What is the language circuit of the brain?

A

Wernicke’s Area:
Anglular Gyrus:
Broca’s Area:

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32
Q

What is processed @ Wernicke’s Area?

A

is the area auditory Input for language is processed– important for Understanding speech

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33
Q

Which brain lobe will you find the Anglular Gyrus and what is its function?

A

it is a part of the temporal Lobe, it combines auditory input from The primary auditory area and other Senses from the somatosensory cortex and visual cortex and feeds into the Wernicke’s area

34
Q

From where does Broca’s Area receive input from? And what does it control? Where does it lie?

A

It receives input from Wernicke’s area and controls the Production of intelligible speech. It lies near the primary motor area that controls the tongue movements that form words – the connection between Broca’s and Wernicke’s area is Bidirectional to facilitate the integration Of speech formation, Comprehension, & editing.

35
Q

What are the 4 key features of the stroke syndrome?

A

1) Sudden onset—The sudden onset of symptoms is documented by the history.
2) Focal involvement of the central nervous system—The site of central nervous system involvement is suggested by the nature of the symptoms and signs, delineated more precisely by the neurologic examination, and confirmed by imaging studies (computed tomography [CT] scans or magnetic resonance imaging [MRI]).
3) Lack of rapid resolution—The duration of neurologic deficits is documented by the history. In the past, the standard definition of stroke required that deficits persist for at least 24 hours to distinguish stroke from transient ischemic attack (discussed later). However, any such time point is arbitrary, and transient ischemic attacks usually resolve within 1 hour.
4) Vascular cause—A vascular cause may be inferred from the acute onset of symptoms and often from the patient’s age, the presence of risk factors for stroke, and the occurrence of symptoms and signs referable to the territory of a particular cerebral blood vessel. When this is confirmed by imaging studies, further investigations can be undertaken to identify a more specific etiology, such as arterial thrombosis, cardiogenic embolus, or clotting disorder.

36
Q

Acute onset

A

Begin abruptly. Neurologic deficits may be maximal at onset, as is common in embolic stroke, or may progress over seconds to hours (or occasionally days), which may occur with progressive arterial thrombosis or recurrent emboli.

37
Q

A transient ischemic attack (TIA) characteristics?

A

produces neurologic deficits that resolve completely within a short period, usually within 1 hour.

38
Q

What is a stroke-in-evolution?

A

or progressing stroke, causes deficits that continue to worsen even as the patient is seen.

39
Q

Defining characteristics of a completed stroke?

A

defined by the presence of persistent deficits, which may be stable or improving when the patient is seen; it does not necessarily imply that the entire territory of the involved vessel is affected or that no improvement has occurred since the onset.Acute Onset Strokes begin abruptly. Neurologic deficits may be maximal at onset, as is common in embolic stroke, or may progress over seconds to hours (or occasionally days), which may occur with progressive arterial thrombosis or recurrent emboli.

40
Q

Most notable s/s associate with anterior circulation ischemia?

A 
Hemi-or monoparesis=38%
Hemisensory defecit=33%
H/A=25%
Aphasia=20%
Visual field defect=14%
Altered LOC=5%
dysarthria=3%
41
Q

Most notable s/s associated with posterior circulation ischemia?

A 
Vertigo=48%
Visual field defect=22%
Altered LOC=16%
Drop attacks=16%
Hemi or monoparesis=12%
Dysarthria=11%
Hemisensory deficit=9%
Diplopia=7%
H/A=3%
42
Q

Meningitis vs. Meningoencephalitis

A

Meningitis is an inflammation of the three membranes that cover the brain and spinal cord (the meninges). Encephalitis is an inflammation of the brain. Meningoencephalitis is an inflammation of both the brain and the meninges.

43
Q

What are the three classifications of meningitis?

A

Three classifications:
1) Acute Pyogenic – bacterial Meningitis-The microorganisms vary with age-Infant – Escheria colia and group B streptococci
Elderly – Streptococus pneumoniae and Listeria monocytogenes
Adolescents and young adults – Neisseria meningitis
2) Aseptic - Viral Meningitis (an enterovirus in 70% of cases)
3)Chronic Meningoencephalitis (viral or bacterial) (usually tuberculosis, syphilis, Lyme disease)

44
Q

Clinical manifestations of meningitis?

A

Most patients have a rapid onset of fever, headache, lethargy, and confusion. Fewer than half complain of neck stiffness, but nuchal rigidity is noted on physical examination in 30–70%. Other clues seen in a variable proportion of cases include altered mental status, nausea or vomiting, photophobia, Kernig’s sign (resistance to passive extension of the flexed leg with the patient lying supine), and Brudzinski’s sign (involuntary flexion of the hip and knee when the examiner passively flexes the patient’s neck). More than half of patients with meningococcemia develop a characteristic petechial or purpuric rash, predominantly on the extremities.

45
Q

What is the mental status of patients infected with meningitis?

A

Although a change in mental status (lethargy, confusion) is common in bacterial meningitis, up to one third of patients present with normal mentation. From 10% to 30% of patients have cranial nerve dysfunction, focal neurologic signs, or seizures.

46
Q

What are the are ominous signs of impending herniation (brain displacement through the foramen magnum with brain stem compression), heralding imminent death?

A

Coma, papilledema, and Cushing’s triad (bradycardia, respiratory depression, and hypertension) are ominous signs of impending herniation (brain displacement through the foramen magnum with brain stem compression), heralding imminent death.

47
Q

What is consciousness?

A

All forms of brain injury and disease can lead to altered levels of consciousness.Consciousness is the state of awareness of self and the environment and of being able to orient to new stimuli.

48
Q

What the two necessary components for consciousness?

A

1) Arousal and wakefulness (requires concurrent functioning of RAS and cerebral cortex)
2) Content and Cognition (requires a functioning cerebral cortex)

49
Q

What are the 5 levels of consciousness?

A 
Confusion 
Delirium  
Obtundation 
Stupor
Coma
50
Q

What are the characteristics of confusion?

A

impaired ability to think clearly, and to perceive, respond to, and remember stimuli (disorientation)

51
Q

What are the characteristics of delirium?

A

motor restlessness, transient hallucinations, disorientation, and sometimes delusions

52
Q

What are the characteristics of obtundation?

A

decreased alertness with associated psychomotor retardation

53
Q

What are the characteristics of stupor?

A

conscious but with little or no spontaneous activity

54
Q

What are the characteristics of coma?

A

unarousable and unresponsive to external stimuli or internal needs often determined by the Glasgow Coma scale

55
Q

How is brain death defined and what must be demonstrated on physical/clinical exam?

A

Is defined as the irreversible loss of function of the brain, including the brain stem.
Clinical examination must disclose at least the absence of responsiveness, brain stem reflexes, and respiratory effort. (repeat evaluation after 6 hours is recommended and use of EEG testing)

56
Q

What is persistent vegetative state characterized by?

A

Persistent Vegetative State is characterized by loss of all cognitive functions and unawareness of self and surroundings. Reflex and vegetative functions remain. Other characteristics include: inability to interact with others, absence of sustained or reproducible voluntary behavioral responses, lack of language comprehension, bowel and bladder incontinence, non-oral feeding, and variably preserved cranial or spinal reflexes (lasting at least 1 month).

57
Q

Most persons in prolonged coma who survive evolve into a

A

evolve into a persistent vegetative state.

58
Q

What are the degenerative diseases of the cerebral cortex, the dementia syndromes?

A 
Alzheimer's disease (AD) 
Vascular dementia (VaD) 
Parkinson's disease with dementia (PDD) 
Frontotemporal dementia (FTD) 
Reversible dementias
59
Q

What type of degenerative disease is Parkinson’s?

A

Degenerative Disease of the Basal Ganglia

60
Q

What is the major symptom of AD?

A

Alzheimer’s Disease: The onset of mental changes is usually insidious - The gradual development of forgetfulness is the major symptom.

61
Q

What follows memory loss/disturbance in AD?

A

Alzheimer’s Disease Clinical Features:
.Once the memory disorder has become pronounced, other failures in cerebral function become increasingly apparent. The patient’s speech and writing is halting because of failure to access the needed word. Vocabulary becomes restricted, and expressive language becomes stereotyped and inflexible.

62
Q

What follows loss of spoken word, expressive language?

A

Alzheimer’s Disease Clinical Features:
Late in the course of the illness, the patient forgets how to use common objects and tools while retaining the necessary motor power and coordination for these activities.Finally, only the most habitual and virtually automatic actions are preserved. Eventually difficulty in locomotion develops, a kind of unsteadiness with shortened steps but with only slight motor weakness and rigidity. Elements of parkinsonian akinesia and rigidity and a fine tremor can be perceived in patients with advanced stages of the disease. Ultimately, the patient loses the ability to stand and walk, being forced to lie inert in bed and having to be fed and bathed, the legs curled into a fixed posture of paraplegia in flexion (in essence, a persistent vegetative state).

63
Q

What is Parkinson’s disease?

A

Is a clinical syndrome of rigidity, bradykinesia, tremor, and postural instability. Involves selective degeneration of monoamine-containing cell populations in the brainstem and basal ganglia, particularly of pigmented dopaminergic neurons of the substantia nigra. In addition, scattered neurons in basal ganglia, brainstem, spinal cord, and sympathetic ganglia contain eosinophilic, cytoplasmic inclusion bodies (Lewy bodies).

64
Q

What is involved with Parkinson’s disease?

A

Involves selective degeneration of monoamine-containing cell populations in the brainstem and basal ganglia, particularly of pigmented dopaminergic neurons of the substantia nigra. In addition, scattered neurons in basal ganglia, brainstem, spinal cord, and sympathetic ganglia contain eosinophilic, cytoplasmic inclusion bodies (Lewy bodies).

65
Q

What are the clinical presentations of Parkinson’s ?

A

Clinical Presentation:
Resting tremors of the hands, jaw, and feet.
Bradykinesia (slow movements) and Akinesia (absence of movements)
Speech difficulties – slowed, slurred, stuttering speech. Altered Gait (Parkinson’s shuffle) – slow, no arm swinging, walk of flat feet
Postural changed – stooped over
Rigidity – joint stiffness, decreased range of motion

66
Q

What type of disease is multiple sclerosis?

A

Demyelinating Diseases

67
Q

What are the features suggestive of multiple sclerosis?

A 
Relapses and remissions 
    Onset between ages 15 and 50    
 Optic neuritis  
   Lhermitte's sign    
 Internuclear ophthalmoplegia 
    Fatigue  
   Uhthoff's phenomenon
68
Q

What is Lhermitte’s sign?

A

Is a sudden sensation resembling an electric shock that passes down the back of the neck and can reach the fingers and toes. Often seen in demylinating conditions

69
Q

What is Uhthoff’s phenomenon or syndrome?

A

also known as Uhthoff’s sign and Uhthoff’s symptom is the worsening of neurologic symptoms in multiple sclerosis (MS) and other neurological, demyelinating conditions when the body gets overheated from hot weather, exercise, fever, or saunas and hot tubs.

70
Q

What is Internuclear ophthalmoplegia (INO)?

A

is a disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction. When an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus.

71
Q

What is not a feature of MS?

A 
Steady progression     
Onset before age 10 or after age 50  
   Cortical deficits such as aphasia, apraxia, alexia, neglect     Rigidity, sustained dystonia   
  Convulsions     
Early dementia  
   Deficit developing within minutes
72
Q

What are the early s/s of MS?

A

Weakness or numbness, sometimes both, in one or more limbs is the initial symptom in about half the patients. Symptoms of tingling of the extremities and tight band-like sensations around the trunk or limbs are common.The resulting clinical syndromes vary from a mere dragging or poor control of one or both legs to a spastic or ataxic paraparesis. The tendon reflexes are retained and later become hyperactive.

73
Q

What is a useful adage in caring for a patient with MS?

A

That the patient with MS presents with symptoms in one leg but with signs in both; the patient will complain of weakness, incoordination, or numbness and tingling in one lower limb and prove to have bilateral Babinski signs and other evidence of bilateral corticospinal and posterior column disease.

74
Q

What are common modes of onset of MS?

A

: (1) optic neuritis,

(2) transverse myelitis,
(3) cerebellar ataxia, and (
4) various brainstem syndromes (vertigo, facial pain or numbness, dysarthria, diplopia).

75
Q

Flexion of the neck may induce a tingling, electric-like feeling down the shoulders and back and, less commonly, down the anterior thighs. This phenomenon is known as the

A

This phenomenon is known as the Lhermitte sign.

76
Q

What are the 4 types of MS?

A

1) Relapsing/remitting MS (RRMS)
2) .Secondary progressive MS (SPMS) always begins as RRMS.
3) Primary progressive MS (PPMS) accounts for ~;15% of cases.
4) Progressive/relapsing MS (PRMS) overlaps PPMS and SPMS and accounts for ~;5% of MS patients.

77
Q

Relapsing/remitting MS (RRMS)

A

accounts for 85% of MS cases at onset and is characterized by discrete attacks that generally evolve over days to weeks (rarely over hours). There is often complete recovery over the ensuing weeks to months. However, when ambulation is severely impaired during an attack, approximately half will fail to improve. Between attacks, patients are neurologically stable.

78
Q

Secondary progressive MS (SPMS)

A

always begins as RRMS. At some point, however, the clinical course changes so that the patient experiences a steady deterioration in function unassociated with acute attacks (which may continue or cease during the progressive phase). SPMS produces a greater amount of fixed neurologic disability than RRMS. For a patient with RRMS, the risk of developing SPMS is ~;2% each year, meaning that the great majority of RRMS ultimately evolves into SPMS.

79
Q

Primary progressive MS (PPMS)

A

accounts for ~;15% of cases. These patients do not experience attacks but only a steady functional decline from disease onset.

80
Q

Progressive/relapsing MS (PRMS)

A

overlaps PPMS and SPMS and accounts for ~;5% of MS patients. Like patients with PPMS, these patients experience a steady deterioration in their condition from disease onset. However, like SPMS patients, they experience occasional attacks superimposed upon their progressive course .

PATHO Neuro (1 decks)

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