Nervous System Flashcards

Question

Are you with me?

Answer 1

1. Space occupying lesions 2. Edema and swelling 3. Hydrocephaly

Answer 2

1. Vascular (vasogenic), most common cause of brain edema, associated with increased vascular permeability 2. Cellular (cytotoxic), increased cell water indicates injury

Answer 3

the volume of CSF is increased, the ventricles are dilated

Answer 4

the ventricles are expanded secondary to atrophy of the brain, therefore there is not an increase in CSF pressure

Answer 5

an imbalance exists between the rates of production (choroid plexus) and absorption (arachnoid granulations)

Answer 6

1. Overproduction of CSF | 2. Decreased transport and/or absorption of CSF

Answer 7

1. CSF does not reach the subarachnoid space since its circulation is blocked internally 2. Congenital anomalies 3. tumors, abscesses and other SOL's 4. Scarring in the ventricular system, obstruction at foramina of Magendie and Luschka

Answer 8

1. CSF enters the subarachnoid space but the circulation or its absorption is blocked 2. Scars of the arachnoid granulations and/or in the meninges (bacterial meningitis, hemorrhages) 3. Thrombi, neoplasms, and other obstructions of cerebral (dural) venous sinuses and associated veins 4. Severe CHF -> venous congestion and pooling

Answer 9

1. Cerebral Aqueduct of Sylvius 2. Foramina of Magendie and Luschka 3. The subarachnoid space between the midbrain and the forebrain

Answer 10

block absorption of CSF in the arachnoid granulations

Answer 11

1. Papilledema ('chocked disc") 2. Herniation: the rigid skull and dural reflections force the brain to be squeezed through openings and around partitions like putty when it is displaced or undergoes sufficient swelling or expansion. 2a. Cingulate (subfalcine) 2b. Uncal (trans-tentorial) 2c. Tonsillar (cerebellar, "coning") - may lead to compression of the medulla at the foramen magnum and is a common mechanism of death in swelling of the brain

Answer 12

1. Headache 2. Mental Dullness 3. Nausea 4. Vomiting

Answer 13

1. Drooling 2. Squinty eyes 3. Forgetting green water bottle places 4. Frustration with fantasy NHL

Answer 14

1. Penetrating and crushing injuries associated with distortion of cranial vault and cerebral column 2. Trauma without damage to cranium 3. Cord trauma

Answer 15

1. Contusion 2. Laceration 3. Concussion 4. Rotary motion 5. Contrecoup injury 6. SUBLUXATION

Answer 16

interstitial bleeding due to blunt trauma (bruise)

Answer 17

To keep their nuts dry!

Answer 18

associated with tearing (damage) of brain surface with bleeding into surrounding region (CSF), trauma also contributes to edema and swelling of affected components

Answer 19

1. A clinical syndrome associated with a closed head injury, usually in the absence of bleeding 2. Effects include loss of consciousness, possible alterations in reflexes 3. The pathogenesis is unclear but may be associated with disturbances to the midbrain reticular activating system 4. Severity is variable but recovery is common

Answer 20

shearing effects

Answer 21

head trauma causes damage to parts of the brain opposite the site of impact

Answer 22

Doesn't need to worry about wet nuts, Kayla's got them.

Answer 23

1. Penetrating and crushing injuries: displacement or distortion of vertebral elements damage cord 2. vertebral dislocations 3. SUBLUXATION

Answer 24

1. stenosis of the vertebral canal | 2. similar skeletal changes

Answer 25

1. Meningitis | 2. Encephalitis

Answer 26

infection of the meninges and CSF

Answer 27

1. infection of meninges and CSF 2. when severe, may present with systemic signs of infection in addition to localizing signs; stiff neck, headaches, photophobia 3. in survivors, meningeal scarring and obstruction of CSF flow may produce complications

Answer 28

1. Acute pyogenic (bacterial) 2. , Acute lymphocytic (viral) 3. Chronic

Answer 29

characterized by purulent exudates in meninges 1. Generally acute clinical course with high mortality 2. Bacterial cause 3. Increased turbidity in CSF

Answer 30

consisting of, containing, or discharging pus

Answer 31

1. N. meningitidis (meningococcus) - most common in adolescents and young adults, especially during epidemics 2. E. coli, H. influenzae, S. pneumoniae and other opportunisitc infections in young and immunodeficients

Answer 32

1. Elevated polys 2. Elevated protein 3. Reduced glucose 4. Bacteria present

Answer 33

1. More common, course is less severe 2. Microbial causes 3. CSF changes

Answer 34

1. Mumps 2. ECHO viruses 3. Epstein-Barr 4. Herpes simplex (type II)

Answer 35

1. Elevated Lymphocytes 2. Moderately elevated protein 3. Normal glucose

Answer 36

1. Course may have insidious origin, progressive headaches, malaise, vomiting, etc. 2. Microbial causes: - Tuberculosis - Fungi - Brucellosis 3. Subarachnoid space is often filled with exudates or becomes fibrotic 4. CSF: increased "mononuclear" cells, markedly elevated protein

Answer 37

infection of brain parenchyma

Answer 38

1. Mononuclear cell infiltrates - interstitial, perivascular 2. Intracellular inclusion bodies - proliferation of viruses 3. Latency is common 4. "Tropism" (selectivity) determines which neurons or parts of the brain are affected 5. Effects range from mild to lethal according to cause and resistance in the host

Answer 39

1. Arbor viruses 2. Childhood infections 3. Herpes simplex types I and II 4. Poliomyelitis 5. Rabies 6. HIV

Answer 40

arthropod borne, most common epidemic forms | also includes equine types (reservoir is birds not horses)

Answer 41

MMR | CNS if likely associated with immune mechanisms

Answer 42

generally affect peripheral nerves but the infection spreads centrally along nerve fibers and reaches the brain on occasion

Answer 43

nearly eradicated in the western hemisphere, but carriers (canadians) for the disease exist

Answer 44

acquired from animal bites, virus follows nerves to brain - 40k deaths/year

Answer 45

60% AIDS patients develop neurologic complications - cognitive and motor dysfunction

Answer 46

characterized by long incubation period and prolonged relentless illness 1. SSPE 2. Progressive multifocal leukoencephalopathy

Answer 47

1. may follow childhood measles | 2. gives rise to dementia and motor disturbances leading to death over a few years

Answer 48

1. In immunosuppressed patients | 2. Oligodendroglia infected

Answer 49

1. Primarily affect the nervous system of humans and animals 2. Microscopic vacuolization of the brain tissue (spongiform degeneration) and the accumulation of abnormal forms of prion proteins (PrP)

Answer 50

1. Creutzfeldt Jacob disease 2. Kuru 3. FFI/MCD

Answer 51

1. "Subacute Spongiform Encephalopathy" - involved areas of gray matter undergo extensive atrophy 2. Initial effects include subtle changes in behavior and memory followed by rapidly progressive dementia (7 months duration) 3. Incidence: 1/1 million. Conrtibutuing factors include spontaneous and hereditary mutations and transmission

Answer 52

1. Corneal transplants 2. Pituitary extracts 3. Ocular instrumentation 4. Cranial surgery 5. Electrode implants 6. Contact with infected tissue

Answer 53

1. Described in the highlands of New Guinea and appears to have been transmitted by cannibalism of infected human brains 2. causative agent and lesions appear to be similar to those observed in Creutzfeldt Jacob disease except that degeneration is most prominent in the cerebellum and corpus striatum 3. Clinical: ataxia leads to motor incapacity and death within one year

Answer 54

1. Fatal familial insomnia - human and scrapie in sheep 2. Chronic wasting disease - deer and elk 3. Mad Cow Disease - bovine spongiform encephalopathy (BSE), possibly transmission to humans through handling and consuming body parts from infected animals

Answer 55

normal membrane glycoprotein that becomes changed to an abnormal isoform in disease; change from a normal alpha-helix to a beta-pleated sheet pattern. abnormal molecules seem to propagate by making contact with normal molecules and inducing them to "refold" into the pathologic configuration. Accumulation of this material appears to be the cause of disease but how this contributes to neuronal damage and eventual cell death is unclear - abnormal proteins are generaly resistant to many agents that normally inactivate viral DNA. These molecules are also more resistant to digestion with proteases but it is reported that phenol and certain other treatments may render this material non-infectious.

Answer 56

Abnormal PrP is transmissible and infectious when inoculated into appropriate hosts Abnormal PrP infects any species that has the gene for PrP Eliminating the gene results in no infection

Answer 57

1. Genetic: hereditary and sporadic mutations of the PrP regulatory gene 2. Environmental: exposure to infected individuals; respiratory dissemination, neurosurgery; or contaminated material; nerve tissue in animal parts, brain tissue, pituitary ext rats, ocular and CNS instrumentation, corneal transplants, etc.

Answer 58

1. Abscess | 2. Granulomas

Answer 59

1. Focal, usually bacterial infection 2. Causes include hematogenous dissemination and local extension 3. during acute stages local destruction and swelling may produce symptoms 4. CSF findings are variable dependent upon location, size, and extension of the infection 5. Repair is associated with vascularized collagenous tissue with risk for adhesions

Answer 60

focal nodular infections consisting of macrophages, giant cells, etx 1. give rise to locally destructive and expansile lesions 2. Causes include TB and Fungi; may extend to meninges

Answer 61

1. Extension from sinus and middle ear infections 2. Hematogenous dissemination 3. Direct invasion: trauma and congenital defects 4. Peripheral nerves: Rabies and Herpes Encephalitis

Answer 62

1. Stroke | 2. Transient Ischemic Attacks

Answer 63

1. Focal loss of neurological function of vascular origin which lasts more than 24 hours or leads to death 2. Spontaneous onset due to underlying CV disease

Answer 64

1. 3rd leading cause of death in industrialized societies 2. the overall mortality during the first month is generally 40-50% 3. neuroligical deficits persist in 60% of survivors

Answer 65

1. Sudden focal and reversible neurological disturbances due to disruption of blood supply which last less than 24 hours. 2. Most of these events are caused by emboli and the risk for stroke in these subjects is about 5%/yr

Answer 66

1. Focal Ischemic Infarcts due to local obstruction of blood supply 2. Spontaneous hemorrhage

Answer 67

1. Account for 75-90% strokes 2. Most are caused by atherosclerotic disease 3. other causes or reduced perfusion include inflammatory arteritis, arterial spasms, and dissecting aneurysms 4. neurons can tolerate up to 3-5 minutes of poor vascular perfusion before permanent damage occurs; however, recent reports describe neuronal deficits during much shorter periods of hypoxia

Answer 68

1. commonly associated with atherosclerotic lesions | 2. frequent locations include carotids, basilar and proximal middle cerebral arteries

Answer 69

1. Thrombi, fragments of athersclerotic plaques 2. Important sources include the arterial supply of the brain and lesions/dysfunction of the left side of the heart 3. Emboli are usually carried into smaller vessels; branches of the middle cerebral artery

Answer 70

1. ischemia of the entire brain; hypotensive events 2. reversible mental confusion to infarction, may involve the entire brain (vegetable state) or may be limited to more susceptible parts or in the "watershed" regions of the brain and spinal cord

Answer 71

discoloration and softening, petechiae may appear in the margins of the affected region

Answer 72

1. Cerebral tissue becomes very soft and begins to break up 2. Edema is also common and when severe, may cause herniation 3. Edema often exacerbates early neurological symptoms but as it diminishes during recovery, function often improves

Answer 73

residual cavity (cyst) surrounded by astrocytes or a collapsed scar is common

Answer 74

1. Intracerebral | 2. Subarachnoid

Answer 75

bleeding withing brain 1. peak incidence: 60 yrs 2. Most cases are due to rupture of small intraparenchymal arteries

Answer 76

1. effects of intersititial hemorrhage include dissection of nerve tissue, mass effects, disruption of blood supply 2. Sometimes blood may reach the subarachnoid space or the ventricles 3. Usually arises suddenly, progression is rapid

Answer 77

1. Arteriolar sclerosis with occlusion os small "penetrating" arteries and arterioles give rise to small lesions known as lacunar infarcts. depending upon location, neurologic symptoms range from absent to severe 2. Rupture of small penetrating arteries may give rise to "slit hemorrhages" 3. Acute hypertensive encephalopathy: diffuse cerebral dysfunction caused by elevated intracranial pressure that requires immediate intervention 4. Multi-infarct dementia: characterized by accumulated effects of repeated brain infarcts due to hypertensive arteriosclerotic disease

Answer 78

1. rupture of congenitial berry aneurysms 2. sudden onset with signs of meningeal irritation 3. CSF findings 1-24 hours: blood "stained" >24 hours: xanthochromia

Answer 79

1. Epidural hematoma 2. Subdural hematoma 3. Head trauma and spinal injury

Answer 80

Cz: rupture or lacerations of the middle meningeal artery Sx: Neurological manifestations are commonly absent during the first few hours - "lucid interval" As hemorrhage progresses an expanding hematoma is produced within a few hours and symptoms associated with elevated intracranil pressure and brain displacement develop. Tx: Immediate surgical intervention is required

Answer 81

Cz: rupture of small communicating veins that course between cortex and the dural venour sinuses, blood accumulates in a "potential space" between the dura and arachnoid Trauma is a common cause; brain atrophy for any reason may lead to stretching of the cerebral veins with an increased vulnerability for rupture. Sx: appear within 48hrs of trauma but are slowly progressive; clinical symptoms are often vaguely localized and include headache and mental confusion

Answer 82

contusions and lacerations of the brain and spinal cord

Answer 83

1. Parkinsonism 2. Dementia 3. Degenerative motor neuron disease

Answer 84

1. Stooped posture 2. festinating gait 3. "cogwheel rigidity" of the limbs 4. sluggish voluntary movement 5. a "Pill-rolling" tremor at rest 6. Rigid and expressionless facial expression

Answer 85

degeneration of the dopamine-producing pigmented neurons of the substantia nigra and locus ceruleus

Answer 86

1. Lewy bodies consisting of filamentous deposits appear in degenerating neurons 2. in H&E stained tissue, these bodies are homogenous and pink in appearance and exhibit a pale halo 3. In Parkinsonism, the pigmented neurons of the substantia nigra are predominantly affected

Answer 87

1. An autosomal dominant gene defect associated with regulation of synuclein - a presynaptic protein. One extra copy leads to parkinsonism w/o dementia, two leads to parkinsonism with lewy body dementia 2. An autosomal recessive gene regulates parkin, an agent that serves to "upiquinate" products associated with synuclein

Answer 88

1. Idiopathic Parkinson's Disease (Paralysis Agitans) 2. Secondary to encephalitis (Influenza), exposure to dopamine antagonists and other agents, vascular disease, multiple head trauma 3. Diffuse Lewy body disease (DLBD)

Answer 89

1. Spontaneouls onset; 50-60 years 2. Pigmented neurons in the substantia nigra and locus ceruleus undergo degeneration with Lewy bodies 3. Cognitive functions usually preserved except ina subset of Parkinson's

Answer 90

1. More common in younger subjects | 2. Less distinctive, depletion of substantia nigra with formation of neurofibrillary tangles is common

Answer 91

associated with degeneration of cortical neurons in addition to the substantia nigra with dementia and Parkinsonism

Answer 92

L-dopa provides symptomatic improvement | Severity of parkinsonism is proportional to dopamine deficiency

Answer 93

1. Diseases of the cortex 2. Mental incompetency in previously normal subjects 3. Effects include memory loss, poor judgment, "delusions of grandeur", disorientation

Answer 94

1. CVA 2. Hydrocephalous 3. Encephalitis 4. Metabolic Disturbances 5. Slow viruses

Answer 95

1. Senile and Presenile patterns 2. Progressive brain atrophy 3. Loss of cortical functions lead to profound dementia, 5-7 years. loss of motor function leads to death

Answer 96

1. Cerebral atrophy (frontal, temporal, parietal) 2. Increased number of neuritic plaques 3. Neurofibrillary tangles 4. Amyloid Angiopathy 5. Granulovacuolar degeneration

Answer 97

1. Composed of tortuous neuronal processes containing abnormal "tau-proteins" that surround a central amyloid core. The amyloid core consists of small peptides, alipoprotein, and other elements.

Answer 98

1. A-beta appears to be neurotoxic or enhances neurotoxicity of some other agent. Amyloid deposits appear to stimulate inflammation, antibodies against amyloid fragments appear to clear away the plaques and proteins against disease 2. Genetic defects in presinilins lead to early onset AD. Presinilins modify activity of one or more of the enzymes that degrade A-beta. 3. Alipoprotein E is a risk factor for late onset AD. APOE accumulates in senile plaques, blood vessels and it seems to contribute to "tangling" of nerve prcesses and serves as a template for beta-pleating.

Answer 99

1. Unknown 2. Aluminum toxicity, slow viruses, prions, hereditary factors 3. Familial defects on chromosomes 21, 1, 14, 19 4. Individuals with Down's syndrome exhibit cortical changes identical to AD

Answer 100

1. UMN 2. LMN 3. Combined

Answer 101

Most common motor neuron disorder, affects both upper and lower motor neurons; sensory elements are generally not affected

Answer 102

1. Loss of motor neurons in the anterior horn cells of the spinal cord, may also involve cranial motor nuclei and UMN (Betz cells) 2. Loss of anterior horn cells leads to muscle atrophy in the hand and other locations 3. Loss of UMNs lead to lateral column degeneration with gliosis

Answer 103

1. Unknown 2. Suspected factors include viruses and metabolic disorders 3. A hereditary form associated with a defective superoxide dismutase gene on chromosome 21 in 10%

Answer 104

cystic expansion of central canal of spinal cord affects "crossing fibers" with segmental motor and sensory deficits

Answer 105

1. MS is the most common of acquired and inherited conditions that affect myelin in the CNS a. US - 250k-500k b. Peak onset 20-40 years of age c. Women 2x d. Most common in Caucasian population

Answer 106

1. Host susceptibility - risk 15x greater in 1st order relatives of patients 2. Exposure to certain infectious agents is suggested and populations living in higher temperate latitudes seem to be at greatest risk a. childhood exposure to infections b. most clear in Europe and North America... yes even Canada

Answer 107

Autoimmunity to components of the myelin sheath contributes to damage. This is associated with patchy demyelinization and glial scarring within the CNS. T and B cell mechanisms implicated

Answer 108

1. Distinct demyelinated plaques originate around venules and veins and progress to reach macroscopic size

Answer 109

1. Optic nerve and chiasm - may cause ocular pain, retinal changes and visual disturbances 2. Periventricular white matter 3. Brain Stem 4. Cerebellar peduncles, dorsal columns of spinal cord

Answer 110

1. Increased fatigability 2. Paresthesia 3. Visual losses and other optic disturbances 4. Locomotor disturbances 5. Depression

Answer 111

1. Acute progressive - 10-20 months survival | 2. Chronic progressive - 20-30 years survival

Answer 112

1. Typical MS 2. Characterized by episodic periods of remission and exacerbation; loss of function progresses with each episode 3. Long survival

Answer 113

1. Sypmtoms 2. CSF 3. CT/MRI 4. Nerve conduction studies

Answer 114

1. Brought on by stress or other illness, increasing body temperatures 2. Stress management therapy, exercise, dietary management 3. Medicinal to "desensitize" and control anti-myelin reations

Answer 115

65% are "functional" at 10 years, and 35-30% after 20 years

Answer 116

1. Paresis 2. Tabes dorsalis 3. Meningeo-vascular lesions

Answer 117

1. Progressive neuronal loss with cerebral atrophy | 2. Clinical effects: dementia, changes in behavior, tremor, memory loss, Argyll-Robertson pupil

Answer 118

1. Fibrosis and gliosis of posterior columns of spinal cord 2. Pathogenesis: poorly defined 3. Sx: variable

Answer 119

1. lightning pains, painful paresthesias 2. ataxia, loss of DTR 3. Visceral effects include bladder dysfunction, episodic abdominal pain and vomiting

Answer 120

chronic meningitis with thickening, obliterative arteritis - gummas may extend into cortex, brain stem or cord

Answer 121

1. Primary Tumors - derivatives of glial elements most common 2. All primary neoplasms arising within the substance of the CNS are potentially life threatening because of their critical location. Also, morphologic distinctions between benign and malignant CNS tumors are often vague and some may change from to a malignant course spontaneously

Answer 122

secondary (metastatic) - includes 25-30% of intracranial tumors, recent reports suggest closer to 50% 1. tends to be multiple 2. most commonly associated with metastasis of malignant melanoma as well as from primary tumors of breast and lung

Answer 123

1. Extra-axial tumors 2. arise outside the CNS 3. cause compression and are more easily removed than those originating within the brain or spinal cord

Answer 124

1. Meninges and epidural structures 2. Nerve sheaths 3. Pituitary 4. Craniopharyngiomas and pineal gland tumors

Answer 125

1. arise within the CNS 2. 70% adult within the cerebral hemispheres 3. 70% children in cerebellum

Answer 126

1. Astrocytoma 2. Glioblastoma multiforme 3. Ependymoma 4. Oligodendroglioma

Answer 127

located in cerebrum, also in cerebellum, brain-stem, and spinal cord

Answer 128

a poorly differentiated, invasive glial cell tumor

Answer 129

derived from the lining of the ventricular system of the brain and the central canal of the spinal cord

Answer 130

uncommon, in some cases the lesions may calcify

Answer 131

1. Most common in children 2-4 yrs | 2. Composed of small, poorly differentiated cells seen most commonly in the crebellum

Answer 132

1. Retinoblastoma - chromosome 13 defect | 2. Neuroblastic tumors - Adrenal medulla, peripheral ganglia, may give rise to intra-axial tumor

Answer 133

1. Regeneration 2. Neuropathy 3. Neuralgia

Answer 134

Limited to peripheral fibers and is dependent upon preservation of the neuriemmal tube

Answer 135

functional/pathological disturbances of peripheral nerves 1. Pathogenesis 2. Distribution 3. Symptoms 4. Etiology

Answer 136

Mechanisms that cause the degeneration of axons and/or loss of myelin 1. Wallerian Degeneration 2. Axonal Degeneration 3. Segmental Demyelination

Answer 137

1. Occurs in distal segment of injured peripheral nerve 2. Typical response to mechanical injury 3. Debris is removed prior to regeneration of peripheral fiber 4. Perikaryon of the injured nerve undergoes swelling, chromatolysis and other acute neuronal stress reaction; recovery depends upon survifval of neuron and a maintained continuity of the neurilemma

Answer 138

1. "Dying back" of affected nerve fibers 2. Seems to reflect an inability of a neuron to maintain its axons 3. Potential causes include metabolic and ischemic conditions that affect the neuron and/or axons 4. Recovery depends upon survival of the neuron and neurilemma

Answer 139

1. Underlying axon is initially preserved 2. Underlying processes appear to be related to metabolic, inflammatory or toxic injurt to the neurilemma 3. The injury is reversible but if repeated or prolonged excessively, the underlying axons will also degenerate

Answer 140

1. Polyneuropathy | 2. Mononeuropathy

Answer 141

1. Affects multiple nerves in a wide pattern 2. Causes tend to be "systemic" in nature 3. Tends to affect the longest neurons most greatly and initially in a symmetrical and peripheral pattern

Answer 142

1. Affects single or isolated group of neurons | 2. Causes include localized mechanical factors and other forms of isolated pathology

Answer 143

1. Peripheral Somatic Nerves | 2. Autonomic Nerves

Answer 144

1. Motor and sensory nerves may be affected selectively or concurrently 2. Affects include motor weaknesses, paralysis, sensory loss and or paresthesia

Answer 145

When affected, may contribute to bowel, bladder, and CV disturbances

Answer 146

1. Trauma 2. Nutritional deficiencies 3. Systemic Disease 4. Toxins 5. Inflammatory Mechanisms

Answer 147

includes compression and entrapment | 1. Demyelination seems to occur initially, followed by axonal degeneration

Answer 148

1. Spinal nerve compression at IVF 2. Radial nerve injury 3. Peroneal nerve injury 4. Ulnar nerve entrapment 5. Carpal tunnel syndrome

Answer 149

Beriberi - B1 | causes myelin degeneration and loss of axons, usually starts in legs

Answer 150

1. Diabetes | 2. Amyloidosis

Answer 151

neuropathy in 50% when the disease has been present for 25 years or more 1. Peripheral vascular disease and hyperglycemia - related metabolic factors 2. Distribution of neurologic manifestations

Answer 152

1. Sensory fibers affected most greatly; particularly those of greatest length: somatic motor fibers may also be ultimately affected 2. Autonomic fibers affected in 20-40% chronic diabetics - contribute to bladder, bowel, and CV disturbances, visceral pain and sweating anomalies

Answer 153

1. Diphtheria 2. Lead 3. Other agents

Answer 154

Endotoxin damages nerves

Answer 155

affects include dysfunction of radial and peroneal nerves; wrist and foot drop

Answer 156

Hg, Uremia, arsenic, etc.

Answer 157

1. Bell's Palsy | 2. Guillain-Barre Syndrome

Answer 158

1. Inflammatory swelling of CN VII of uncertain origin | 2. Leads to nerve compression and weakness of facial muscles - usually lasts 4-8 weeks 75% recovery

Answer 159

1. Most common acute paralytic disease of young adults in US 2. Pathogenesis uncertain but immunological mechanisms are implicated in most cases About 2/3 follow acute flu-like illness EBV, vaccination, HIV, surgery, lymphomas

Answer 160

1. Inflammatory cells and segmental demyelination; lymphocytes and monocytes, axonal degeneration 2. Large nerves affected most extensively; spinal roots, plexuses, nerve trunks

Answer 161

Usually acute with rapid progression of weakness from distal to proximal muscle groups 1. Dominated by ascending paralysis of lower extremities, may progress to variably affect trunk, arm, and facial muscles 2. When severe, respiration, swallowing, and visceral autonomics may be affected - 2-5% die of complications 3. Paresthesia is also common but is less dominating 4. Recovery begins within 2-4 weeks, 85% are ambulatory at 6 months

Answer 162

Pain 1. Nerve Trauma or Compression 2. Inflammation (neuritis) 3. Idiopathic: tix douloureux <- what a canadian word!

Answer 163

1. Shingles (Herpes Zoster) | 2. Herpes Simplex

Answer 164

Herpes Zoster 1. Associated with latent infection of DRG 2. Episodic flare-ups with painful segmental cutaneous vesicular eruptions

Answer 165

1. Type I (above waist) - cold sores 2. Type II - genital herpes 3. Leads to vesicular lesions in skin and mucus membranes at site of initial exposure and infects neurons that innervate these locations

Answer 166

1. Epithelial lesions heal 2. Infection remains latent in neurons and may be episodically reactivated and produce more lesions 3. Type I commonly localizes in sensory component of CN V, involvement of opthalmic division may cause corneal lesions. In infants and immunosuppressed, control is reduced and the infection may follow nerve fibers into the brain and cause encephalitis

Answer 167

1. Spontaneous episodes of lightning pain affecting one or more divisions of CN V 2. Tx include sectioning portions of the CN V or its sensory pathways, relief of compression and certain drugs

Answer 168

1. Attacks may be precipitated by light stimulation of skin of face or in mouth - touching, brushing, talking, and eating - episodes may last a few seconds at a time and may be extremely painful 2. Underlying cause unclear a. compression of portions of V seen in some, ganglion tumors may be responsible in others b. Structural lesions are not always seen.