Neuro Flashcards
(431 cards)
1
Q
What is the risk level for patients with a history of headache without RED FLAG symptoms?
A
They are at low risk of serious headache.
2
Q
What are the three populations for headaches?
A
- Outpatient office - usually migraine or tension.
- ER - must immediately exclude life-threatening headaches.
- Headaches during pregnancy.
3
Q
What are the two types of headaches?
A
Primary and secondary headaches.
4
Q
What criteria are helpful for identifying red flags in headaches?
A
SSNOOP criteria.
5
Q
What does the ‘S’ in SSNOOP stand for?
A
Systemic symptoms (fever, weight loss).
6
Q
What does the ‘S’ in SSNOOP refer to?
A
Secondary risk factors/underlying disease (HIV, cancer).
7
Q
What does the ‘N’ in SSNOOP stand for?
A
Neurologic signs/symptoms (confusion, focal neuro findings).
8
Q
What does the ‘O’ in SSNOOP refer to?
A
Onset (sudden, abrupt).
9
Q
What does the ‘O’ in SSNOOP refer to?
A
Older age (new onset/progressive).
10
Q
What does the ‘P’ in SSNOOP stand for?
A
Pattern change (change from previous in frequency or severity).
11
Q
What is the International Headache Society classification of headaches?
A
Primary Headaches: Migraine, Tension, Cluster, Other (cough, exercise, post coital).
Secondary Headaches: Traumatic, Vascular (TIA, CVA), Substance or substance withdrawal (CO, alcohol, NSAID withdrawal), Infectious (meningitis, influenzas), Disorder of homeostasis (HTN, altitude, sleep apnea/hypoxia), Attributed to disorder of eyes, ears, sinuses, teeth.
12
Q
What are examples of psychiatric disorders related to headaches?
A
Somatization, psychotic disorder.
13
Q
What are examples of painful cranial neuropathies/facial pain?
A
Trigeminal neuralgia, optic neuritis.
14
Q
What is the most common primary headache disorder?
A
Tension Headache
15
Q
What are the two types of Tension Headaches?
A
Episodic (14 or less/month) and Chronic (>15/month)
16
Q
What is the mean age at onset for Tension Headaches?
A
25-30 years
17
Q
At what age is the peak prevalence of Tension Headaches?
A
30-39 years
18
Q
What are some risk factors for Tension Headaches?
A
Stress, Emotional disturbance, Too little sleep, Eye strain/glare, Noise, TMJ
19
Q
What are the peripheral mechanisms involved in Acute Tension Headaches?
A
Muscle tension, nociception, and peripheral sensitization
20
Q
What are the central mechanisms involved in Chronic Tension Headaches?
A
Central sensitization and reduced pain inhibition
21
Q
What psychosocial factors are common comorbidities with Tension Headaches?
A
Stress, anxiety, and depression
22
Q
Which neurotransmitters are involved in Tension Headaches?
A
Serotonin (5-HT), Endorphins, and Dopamine
23
Q
What are the symptoms of Tension Headaches?
A
Bilateral head pain of mild-moderate intensity with a pressing or tightening quality. Pain may be described as ‘band around the head’.
24
Q
What is the most common abnormal finding on exam for Tension Headaches?
A
Pericranial muscle tenderness on palpation (trigger point)
25
What is the diagnostic method for Tension Headaches?
Clinical diagnosis; absence of nausea and vomiting, aided by patient headache diary recorded over > 4 weeks
26
What is the first line treatment for acute Tension Headaches?
Simple analgesics and NSAIDs
27
What is the treatment of choice for Tension Headaches?
Ibuprofen 200-800 mg due to favorable side effect profile
28
What are other options for acute treatment of Tension Headaches?
Naproxen (Aleve), Aspirin, APAP if unable to take NSAIDs (not as effective)
29
What is a second-line option for acute Tension Headaches?
Combination analgesics containing caffeine 64-200 mg
30
What parenteral therapies have evidence of efficacy for Tension Headaches?
Ketorolac, Metoclopramide (N/V), Chlorpromazine (antipsychotic for nausea/vomiting)
31
What is the recommendation for the use of drugs to treat acute Tension Headaches?
Limit use to 2-3 days/week
32
What is the first line for prophylaxis of Tension Headaches?
Amitriptyline
33
What is a migraine?
A primary, episodic headache disorder characterized by unilateral, pulsating pain lasting 4-72 hours, which may have an aura.
34
What are the risk factors associated with migraines?
Family history of migraine and migraine with aura, which is a risk factor for stroke.
35
What is the pathophysiology of migraines?
Altered functional connectivity of the cortex, thalamus, hypothalamus, brainstem, amygdala, and cerebellum, along with central sensitization of the trigemino-cervical complex and abnormal serotonin metabolism.
36
What are the common symptoms of a migraine?
Symptoms last 4-72 hours and include a pulsatile, pounding, or throbbing quality, aggravated by routine physical activity, and may include nausea, vomiting, photophobia, or phonophobia.
37
How are migraines diagnosed?
Migraines are diagnosed clinically. Aura may include visual, sensory, or language disturbances that precede or occur during the headache, lasting 5-60 minutes. No imaging or labs are needed except to rule out secondary headaches.
38
What imaging is used in the ER for migraines?
CT is used in the ER, while MRI is the most sensitive and specific test.
39
What is the treatment for mild to moderate migraines?
Aspirin, Ibuprofen/Naproxen, Acetaminophen (if unable to take aspirin or ibuprofen), Metoclopramide po, and Caffeine.
40
What is the treatment for moderate to severe migraines at home or in the office?
Triptans, Metoclopramide, and Dexamethasone may help to prevent recurrence.
41
What is the treatment for moderate to severe migraines in the ER?
Sumatriptan IM, Ketorolac IM or IV, Metoclopramide IM or IV, and Diphenhydramine (IM or IV).
42
What are the options for migraine prophylaxis?
Antiepileptics (topiramate or valproic acid), Beta-blocker (propranolol), Antidepressants (amitriptyline), and Botulinum toxin. Avoid opioids and barbiturates.
43
What is Cluster Headache?
A primary headache disorder characterized by attacks of severe unilateral pain with ipsilateral autonomic symptoms.
44
What are common triggers for Cluster Headaches?
Triggers include lack of sleep, alcohol (especially red wine), volatile odors, nitrate ingestion (processed meats), and weather changes.
45
What is a nickname for Cluster Headaches?
Nicknamed 'suicide headaches'.
46
What is the typical demographic for Cluster Headaches?
Affects individuals aged 10-39 years, predominantly men, with a history of tobacco use in 73% of cases.
47
What is the pathophysiology of Cluster Headaches?
Involves hypothalamic activation and trigeminovascular system activation, leading to intense unilateral pain.
48
What autonomic symptoms are associated with Cluster Headaches?
Symptoms include lacrimation, nasal congestion, rhinorrhea, ptosis, and miosis (Horner’s syndrome).
49
How long do Cluster Headache attacks typically last?
Attacks usually last 15-180 minutes.
50
What are the characteristics of episodic clusters in Cluster Headaches?
Episodic clusters consist of daily headaches lasting 7 days to 1 year, followed by remission periods lasting months to years.
51
What is Horner Syndrome?
A classic neurologic syndrome characterized by miosis, ptosis, and anhidrosis on the affected side.
52
How are Cluster Headaches diagnosed?
Diagnosis is clinical.
53
What is the first line treatment for Cluster Headaches?
Abortive therapy includes 100% O2 at 6-12 L/minute via high-flow mask with the patient in a sitting position and triptans.
54
What are some prophylactic therapies for Cluster Headaches?
Prophylactic therapy includes Verapamil, monoclonal antibody (Galcanezumab), and Lithium (usually used for bipolar disorder).
55
What is cough-induced Cluster Headache?
Usually only lasts a few minutes after coughing.
56
What is exercise-induced Cluster Headache?
Can last up to a few hours after strenuous exercise.
57
What is post-coital Cluster Headache?
A sudden, severe, throbbing headache that occurs just before or at the moment of orgasm.
58
What is Multiple Sclerosis?
A demyelinating disease of the central nervous system.
59
Who is more commonly affected by Multiple Sclerosis?
Women.
60
What are some risk factors for Multiple Sclerosis?
Low UV light exposure, smoking, obesity (especially during childhood and adolescence).
61
What are the typical patterns of Multiple Sclerosis?
Relapses and remissions.
62
What is Lhermitte’s sign?
A sudden sensation that passes from the back of the neck and down the spine.
63
What is the pathophysiology of Multiple Sclerosis?
Myelin sheath degeneration throughout the nervous system.
64
What are common symptoms of Multiple Sclerosis?
Limb weakness, numbness, abnormal sensations, urination or bowel movement problems, vision problems, gait impairment.
65
What can be a presenting symptom of Multiple Sclerosis?
Optic neuritis.
66
How does heat affect Multiple Sclerosis symptoms?
Heat exacerbates the symptoms.
67
What physical exam findings are associated with Multiple Sclerosis?
Muscle weakness, flaccid muscle tone in acute setting, reduced or abnormal sensations.
68
What is a key diagnostic requirement for Multiple Sclerosis?
Involvement of ≥ 2 areas of the central nervous system at different time points.
69
What laboratory tests are used in the diagnosis of Multiple Sclerosis?
CBC, ESR/CRP, LFT, BUN/Creatinine, Calcium, glucose, thyroid function, vitamin B12, HIV.
70
What imaging study is used to diagnose Multiple Sclerosis?
MRI will show lesions typical of MS.
71
What does CSF analysis show in Multiple Sclerosis?
Oligoclonal bands (IgG) - TEST OF CHOICE.
72
What is the treatment for Multiple Sclerosis?
Interferons and monoclonal antibodies; steroids for acute episodes may be helpful.
73
What are some symptomatic management options for fatigue in Multiple Sclerosis?
Amantadine, modafinil.
74
What are some symptomatic management options for spasticity in Multiple Sclerosis?
Baclofen, tizanidine.
75
What is a treatment option for bladder dysfunction in Multiple Sclerosis?
Anticholinergics.
76
What is a treatment option for depression in Multiple Sclerosis?
SSRIs.
77
What type of support is recommended for patients with Multiple Sclerosis?
Multidisciplinary support including physical therapy and occupational therapy.
78
What is Myasthenia Gravis?
An autoimmune disorder affecting the neuromuscular junction.
79
In which age group is Myasthenia Gravis more common in females?
In patients under 50 years old.
80
In which age group is the initial diagnosis of Myasthenia Gravis slightly more common in males?
In patients over 50 years old.
81
What other autoimmune disorders are associated with Myasthenia Gravis?
Thyroiditis, SLE, and Rheumatoid arthritis.
82
What percentage of Myasthenia Gravis cases are associated with thymoma?
15% of cases.
83
What is the pathophysiology of Myasthenia Gravis?
Antibodies against the acetylcholine receptors.
84
What are the symptoms of Myasthenia Gravis?
Muscle strength is nearly normal in the morning, with weakness and fatigue increasing during the day.
85
Which eye muscles are commonly impaired in Myasthenia Gravis?
Extraocular muscles and orbicularis oculi.
86
What is the 'peek' sign in Myasthenia Gravis?
It is a manifestation of orbicularis weakness.
87
What is the diagnostic test for Myasthenia Gravis?
Testing for acetylcholine receptor (AChR), muscle-specific tyrosine kinase (MuSK), or lipoprotein receptor-related protein 4 (LRP4) antibodies.
88
What is the purpose of the edrophonium chloride (Tensilon) test?
It results in unequivocal resolution of weakness (rarely used).
89
What imaging is done to look for thymus tumors in Myasthenia Gravis?
CT of the chest.
90
What should be avoided in the treatment of Myasthenia Gravis?
Many drugs that may induce or exacerbate the condition.
91
What is the first-line treatment for Myasthenia Gravis?
Acetylcholinesterase inhibitors.
92
Name two acetylcholinesterase inhibitors used in Myasthenia Gravis.
Pyridostigmine and Neostigmine.
93
What is the treatment for exacerbations and severe disease in Myasthenia Gravis?
Immunoglobulin can be given.
94
What is required in a Myasthenic crisis?
Intubation and ICU admission.
95
What percentage of patients experience respiratory failure due to myasthenic weakness?
About 20% of patients, usually within the first year of illness.
96
What is Amyotrophic Lateral Sclerosis (ALS) also known as?
Lou Gehrig’s Disease
97
What is the age range most common for ALS onset?
50-75 years
98
What percentage of ALS cases are idiopathic?
95%
99
What percentage of ALS cases are familial?
5%
100
What are the key genetic variants associated with familial ALS?
C9orf72, TARDBP, SOD1, or FUS genes
101
What is the role of upper motor neurons in ALS?
Responsible for spasticity and clumsiness
102
What is the role of lower motor neurons in ALS?
Responsible for disabling weakness
103
What are common symptoms of ALS?
Muscle weakness, respiratory impairment, slow or slurred speech, emotional lability, cognitive and behavioral symptoms
104
What physical exam signs should be looked for in ALS?
Weak neck flexors/extensors, weak diaphragm, limb weakness, atrophy, fasciculations, spasticity, abnormal reflexes
105
What diagnostic criteria suggest ALS?
Simultaneous upper and lower motor neuron involvement with progressive weakness and exclusion of alternative diagnoses
106
What tests can provide evidence for ALS diagnosis?
Electromyography (EMG), Nerve conduction testing, MRI
107
What tests are used to rule out other diseases?
CSF analysis and Muscle biopsy
108
What are the FDA approved medications for ALS treatment?
Riluzole and Edaravone
109
How do Riluzole and Edaravone affect ALS progression?
They may slow progression and increase life expectancy by 2-3 months
110
What is important to discuss early in ALS treatment?
End of life discussions
111
What does thunderclap denote?
Thunderclap denotes a sudden onset type of headache.
112
What is delirium?
Delirium is typically caused by acute illness or drug toxicity and is often REVERSIBLE.
## Footnote
It is an acute confusional state that fluctuates over hours to days.
113
What are the types of delirium?
Delirium can be hyperactive (DELIRIUM TREMENS) or hypoactive (benzodiazepine overdose).
114
What are the symptoms of delirium?
Symptoms include deficit of attention, memory loss, difficulty with executive function, visuospatial tasks, and language.
## Footnote
Associated symptoms may include altered sleep-wake cycles, perceptual disturbances, and affect changes.
115
What are the risk factors for delirium?
Estimates of delirium in hospitalized patients range from 10 to >50%, with higher rates in elderly patients and those undergoing hip surgery.
116
What percentage of delirium cases in the elderly are due to medications?
1/3 of cases of delirium in the elderly are due to medications.
117
When may symptoms of delirium occur more frequently?
Symptoms of delirium may occur more at night (sundowning).
118
What are the diagnostic criteria for delirium according to DSM-5?
Disturbance in attention and awareness; MUST FIND THE CAUSE.
119
What is the treatment for delirium?
Treatment is based on etiology and may include antipsychotics (haloperidol) and benzodiazepines (Lorazepam).
120
What is dementia?
Dementia is typically caused by anatomic changes in the brain, has a slower onset, and is generally IRREVERSIBLE.
121
What are some types of dementia?
Types of dementia include Alzheimer Disease, Vascular Dementia, Pick’s Disease (frontotemporal dementia), and Diffuse Lewy Body Disease.
122
What are the risk factors for dementia?
Sleep deprivation and swing schedules, traumatic brain injury, social isolation.
123
What are the memory impairments associated with dementia?
Aphasia, apraxia, agnosia, and impaired executive function.
124
What is aphasia?
Typically, word finding difficulty.
125
What is apraxia?
Inability to perform previously learned tasks.
126
What is agnosia?
Inability to recognize objects.
127
What does impaired executive function reflect?
Poor abstraction, mental flexibility, planning, and judgment.
128
What are some symptoms of dementia?
Orientation, cognition, attention, speech and language, recent and remote memory, visuospatial function, mood/personality, and executive functioning.
129
How can recent memory be tested?
By asking the patient to recall a list of ≥ 3 words after 3-5 minutes.
130
What is a common diagnostic tool for dementia?
Mini mental status examination.
131
What is a key treatment approach for dementia?
Provide structure and routine.
132
What should caregivers do when interacting with dementia patients?
Speak simply and break down activities into simple component tasks.
133
What is Alzheimer's disease characterized by?
Abnormal tau proteins, mitochondrial dysfunction, neuroinflammation, oxidative damage, and amyloid-beta plaques.
134
What are common symptoms of Alzheimer's disease?
Personality changes, behavioral difficulties, hallucinations, delusions, and short-term memory loss.
135
What characterizes end-stage Alzheimer's disease?
Near-mutism, inability to sit up or hold head up, difficulty with eating or swallowing, weight loss, and incontinence.
136
What are the diagnostics for Alzheimer's disease?
Low beta-amyloid levels in CSF, PET scan showing beta-amyloid deposits, and MRI showing brain atrophy.
137
What treatments are available for Alzheimer's disease?
Cholinesterase inhibitors and NMDA receptor antagonists.
138
What causes vascular dementia?
Interruption of blood flow to the brain leading to neuronal death.
139
What are the types of vascular brain injuries?
Multi-infarct dementia, subcortical ischemic vascular disease, strategic infarct dementia, hemorrhagic lesions, and hypoperfusion injury.
140
What are the symptoms of vascular dementia?
Executive dysfunction and connectivity problems between brain regions.
141
What diagnostics are used for vascular dementia?
MRI shows infarcts.
142
What is the treatment for vascular dementia?
Treat blood pressure and use anticoagulants as indicated for stroke risk factors.
143
What is Lewy Body Dementia characterized by?
Abnormal inclusion bodies called Lewy bodies found in the cerebral cortex.
144
What are the symptoms of Lewy Body Dementia?
Fluctuating symptoms, rigidity, bradykinesia, and visual hallucinations.
145
What diagnostics are used for Lewy Body Dementia?
MRI with brain atrophy and CSF with increased tau protein.
146
What treatments are available for Lewy Body Dementia?
Cholinesterase inhibitors, antipsychotics for behavior changes, and benzodiazepines for sleep disorders.
147
What is Frontotemporal Dementia?
A type of dementia that occurs in younger patients, with a mean age of onset of 58.
## Footnote
Highly heritable and characterized by abnormal inclusions in the frontal and temporal lobes.
148
What are the symptoms of Frontotemporal Dementia?
Symptoms include apathy, emotional blunting, disinhibition, hyperorality, impaired empathy, and compulsive/repetitive behaviors.
149
How is Frontotemporal Dementia diagnosed?
Diagnosis is made using MRI, which shows brain atrophy.
150
What is the treatment for Frontotemporal Dementia?
Antipsychotics are used to manage behavior changes.
151
What is Essential Tremor?
The most common movement disorder characterized by intention tremors, which occur when trying to do or reach for something.
152
What is the progression and age distribution of Essential Tremor?
It is slowly progressive and benign, with a bimodal peak at age 20 and after 65 years old. It can also occur in children with a mean age of 8.
153
What is a risk factor for Essential Tremor?
Family history, following an autosomal dominant pattern.
154
How does alcohol affect Essential Tremor?
Essential Tremor improves with alcohol, as it acts as a GABA agonist.
155
What is the pathophysiology of Essential Tremor?
Neurodegeneration involving the cerebellum and abnormal GABA function, leading to reduced tone and degeneration of GABA-producing cells.
156
What are the symptoms of Essential Tremor?
Symptoms can be postural or intention tremors and may include a head tremor.
157
How is Essential Tremor diagnosed?
Diagnosis follows the IPMDS diagnostic criteria, requiring bilateral upper limb action tremor for ≥ 3 years without other neurological signs.
158
What is the treatment for Essential Tremor?
Consider medication therapy if tremor interferes with daily activities. First line treatment is Propranolol; second line includes benzodiazepines, gabapentin, and botulinum toxin (Botox).
159
Does Essential Tremor impact life expectancy?
No, it does not impact life expectancy.
160
What is Parkinson's Disease?
A progressive movement disorder characterized by bradykinesia, resting tremor, muscular rigidity, and loss of postural reflexes.
161
Who is most commonly affected by Parkinson's Disease?
Males and older adults.
162
What are some environmental factors associated with Parkinson's Disease?
Consumption of well water and exposure to pesticides.
163
What medications can contribute to Parkinson's Disease?
Antipsychotics.
164
What is the pathophysiology of Parkinson's Disease?
Degeneration of dopamine neurons in the substantia nigra leads to dopamine depletion in the striatum and characteristic motor symptoms.
165
What are the key symptoms of Parkinson's Disease?
Rigidity, postural instability, bradykinesia, and resting tremor.
166
What is a common diagnostic test for Parkinson's Disease?
Patient will have a good response to test dose of Levodopa.
167
What is the first-line treatment for Parkinson's Disease?
Carbidopa/Levodopa, but patients are typically on multiple medications.
168
What non-pharmacologic treatments are recommended for Parkinson's Disease?
Physical/occupational therapy, Tai Chi, exercise, and counseling.
169
What is Huntington Disease?
A rare autosomal dominant neurodegenerative disorder characterized by progressive motor, cognitive, and psychiatric dysfunction.
170
What is the usual age of onset for Huntington Disease?
30-50 years old.
171
What is the pathophysiology of Huntington Disease?
The gene that codes for glutamine repeats too many times, causing excess glutamate production that settles in the basal ganglia.
172
What are the symptoms of Huntington Disease?
Chorea, impaired fine motor skills, and psychiatric symptoms such as depression and anxiety.
173
What is chorea?
A hyperkinetic movement disorder characterized by involuntary brief, random, and irregular contractions.
174
How is Huntington Disease diagnosed?
Diagnosis is confirmed by DNA analysis and MRI evaluates caudate nucleus atrophy.
175
What treatments are available for Huntington Disease?
Tetrabenazine and deutetrabenazine for chorea, Haloperidol for behavioral disturbances, and SSRIs for depression.
176
What supportive care is recommended for Huntington Disease?
Physical therapy, occupational therapy, speech therapy, nutritional support, and palliative care.
177
What is Cerebral Palsy?
A complex group of persistent non-progressive disorders involving movement or posture and motor function including spasticity, dyskinesia, hypotonia, and ataxia due to damaged brain tissue from various perinatal or neonatal causes.
178
What is the incidence of Cerebral Palsy?
2 cases per 1,000 newborns for more than 30 years.
179
What are the risk factors for Cerebral Palsy?
Prenatal exposure to toxins or inflammation, fetal growth restriction, birth defects and congenital malformations, genetic disorders, premature or postdates delivery, low birth weight/small for gestational age, meningitis.
180
What are the TORCH diseases passed by vertical transmission?
Toxoplasmosis, Rubella, Cytomegalovirus, Herpes simplex virus (HSV), syphilis, Zika virus, and HIV.
181
What are the symptoms of Cerebral Palsy?
History of non-progressive motor problems including difficulty with swallowing, motor delay, muscle tone abnormalities, and abnormalities in gait and ambulation.
182
What is the usual age range for the presentation of first clinical signs of Cerebral Palsy?
1 week to 36 months old, with a mean age of 19 months.
183
What are common motor delays in children with Cerebral Palsy?
Not sitting by 8 months, not walking by 18 months, and early hand preference before age 1 year.
184
What is the recommended diagnostic approach for Cerebral Palsy?
Developmental Monitoring and Developmental Screening at 9, 18, and 24-30 months.
185
What is the recommended treatment for Cerebral Palsy?
Refer children for evaluation and treatment as soon as any signs are present, with an integrated, coordinated multidisciplinary care plan.
186
What is Restless Leg Syndrome?
A neurologic disorder characterized by the irresistible urge to move the legs, usually worsening at rest and relieved with movement.
187
What age group is most affected by Restless Leg Syndrome?
Most often occurs in individuals over 65 years old.
188
What factors may exacerbate Restless Leg Syndrome?
Antihistamines, antidepressants, lithium, beta blockers, serotonin reuptake inhibitors, anticonvulsants.
189
What are the underlying factors for Restless Leg Syndrome?
Genetic predisposition, iron deficiency, chronic renal insufficiency, pregnancy, thyroid dysfunction, and certain medications.
190
What is the diagnostic approach for Restless Leg Syndrome?
Iron studies are recommended due to a potential relationship with iron deficiency.
191
What is the 'levodopa' test?
A single dose of levodopa will reduce symptoms for about 2 hours but has a rebound effect, worsening symptoms after use.
192
What are the treatment options for Restless Leg Syndrome?
Treatment of underlying issues, avoidance of alcohol, caffeine, nicotine, sleep hygiene, and gabapentin/pregabalin as first-line treatment.
193
What is the pathophysiology of Cerebral Palsy?
Some room for repair, but not full repair
194
What is Bell Palsy?
Weakness of the 7th cranial nerve, also known as facial nerve palsy.
195
What are the potential causes of Bell Palsy?
It may be idiopathic or secondary to herpes infections.
196
What is the age range with the highest incidence of Bell Palsy?
The highest incidence is between ages 15 and 45 years.
197
What infections are associated with Bell Palsy?
Herpes simplex 1 (most common), varicella zoster, Lyme disease, Epstein Barr.
198
What is the pathophysiology of Bell Palsy?
Some motor neurons to the forehead cross sides at the level of the brainstem, so the fibers in the facial nerve going to the forehead come from both cerebral hemispheres.
199
What happens with supranuclear lesions affecting the facial nerve?
They will not paralyze the forehead on the affected side, resulting in unilateral facial paralysis with forehead sparing.
200
What are the common symptoms of Bell Palsy?
Facial weakness (usually unilateral), unilateral loss of taste sensation, hyperacusis, and a stiff or heavy feeling in the face.
201
What diagnostics are used for Bell Palsy?
No testing needed unless there is suspicion of an underlying disease. Complete blood count, test for syphilis, HIV test, fasting glucose, Lyme titer, and antinuclear antibody titer may be performed.
202
What is the treatment for Bell Palsy?
Eye protection and artificial tears, steroids (usually prednisone) within 3 days of onset, and +/- antivirals for severe palsy.
203
What is Diabetic Peripheral Neuropathy?
Peripheral neuropathy resulting from damage to the peripheral nervous system, affecting up to 50% of patients with diabetes.
204
What types of diabetes can be associated with Diabetic Peripheral Neuropathy?
Can be associated with Type I or Type II diabetes.
205
What leads to the pathophysiology of Diabetic Peripheral Neuropathy?
Intracellular hyperglycemia leads to mitochondrial dysfunction, increased oxidative stress, and increased inflammatory injury.
206
What are the symptoms of Diabetic Peripheral Neuropathy?
Pain (burning, lancinating, electric shock-like, or stabbing) and impaired sensation (numbness or tingling).
207
What physical examination findings are associated with Diabetic Peripheral Neuropathy?
Look for impaired sensations in feet, starting assessments at distal hallux of both feet and moving proximally.
208
How is Diabetic Peripheral Neuropathy diagnosed?
Diagnosis can be made clinically based on pain and impaired sensations, painless foot ulcers, physical signs of impaired sensation, and blood glucose and Hemoglobin A1C.
209
What is the key to treating Diabetic Peripheral Neuropathy?
Prevention is key; optimize glucose control.
210
What are the first-line medications for Diabetic Peripheral Neuropathy?
OTC pain relievers are first line, but pain can be difficult to control.
211
What are the second-line medications for Diabetic Peripheral Neuropathy?
Pregabalin (Lyrica), Duloxetine (Cymbalta), and Gabapentin (Neurontin).
212
postural tremor and causes
patient holds out arms.
Causes: physiologic tremor
Drugs (caffeine/nicotine)
Alcohol withdrawl
increased metabolism
essential tremor
213
Resting tremor and causes
examined at rest
causes: parkinson's disease
drug-induced parkinsonism
supranuclear palsy
214
action (intention) tremor and causes
can be examined at any stage of movement
causes: cerebellar lesions (Stroke, mass)
multiple scleoris s
chronic alcohol abuse
215
Bell's Palsy is idiopathic meaning
it is not associated with truama or other initiating factors. It is overstimulation of cranial nerve 7 (aka the facial nerve) after some type of viral infection.
216
Bells Palsy patients may have dry mouth, eyes, and nose, why?
the facial nerve innervates the sublingual, submandibular glands, lacrimal glands, and mucous membranes of the nasopharynx
217
Bells Palsy patients may also have difficulty earing, why?
the facial nerve innervates the stapesdius muscle of the ear which dampens vibrations.
218
facial nerve innervates what protion of the tongue?
anterior 2/3 of the tongue
219
What is Bell's palsy?
Idiopathic facial nerve paralysis is referred to as Bell’s palsy, characterized by slack muscles of facial expression with gradual return of function over time.
220
What is Guillain-Barré Syndrome?
An acute idiopathic polyneuropathy and demyelinating disease of the peripheral nervous system.
221
What is the most commonly reported preceding infection for Guillain-Barré Syndrome?
Campylobacter jejuni infection.
222
What are some other infections that have been reported before Guillain-Barré Syndrome?
COVID-19 (novel coronavirus) infection.
223
How do symptoms of Guillain-Barré Syndrome progress?
Symptoms progress over 2-4 weeks to potentially life-threatening severity requiring mechanical ventilation before improving or plateauing for weeks-to-months.
224
In which demographic is Guillain-Barré Syndrome slightly more common?
In men and as people get older.
225
What is the proposed mechanism of autoimmune response in Guillain-Barré Syndrome?
There is something on the axon/myelin sheath that appears to the immune system as an antigen, similar to previous infection.
226
What is the symptom progression pattern in Guillain-Barré Syndrome?
Symptoms usually start in distal portions of the legs and are symmetrical.
227
What autonomic dysfunctions are common in Guillain-Barré Syndrome?
Cardiac arrhythmia, excessive sweating, nausea, abdominal pain, constipation, urinary retention.
228
What diagnostic test shows elevated protein levels in Guillain-Barré Syndrome?
Cerebrospinal fluid (CSF) analysis.
229
What is the recommended treatment for Guillain-Barré Syndrome?
Hospital admission, monitoring respiratory function, and starting immunoglobulin or plasmapheresis immediately upon diagnosis.
230
What percentage of Guillain-Barré Syndrome patients report full recovery or only minor deficits?
87% of patients, usually within 1-3 years of onset.
231
What is a seizure?
A transient occurrence of signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.
232
What defines epilepsy?
A condition in which a person has a risk of recurrent seizures due to a chronic, underlying process.
233
What is a tonic seizure?
A seizure that causes sudden stiffness or tension in the muscles of the arms, legs, or trunk.
234
What is an atonic seizure?
A seizure where muscles relax.
235
What is a clonic seizure?
A seizure characterized by fast rapid contraction of the muscles.
236
What are focal seizures?
Seizures that arise from a neuronal network either discretely localized within one brain region or more broadly distributed within a cerebral hemisphere.
237
What is a simple focal seizure?
A seizure affecting one part of one side of the brain where the patient does not lose consciousness.
238
What is a complex focal seizure?
A seizure that occurs on one side of the brain but spreads more throughout, causing altered mental status and loss of consciousness.
239
What is an absence seizure?
Also known as petit mal, it typically occurs in kids around 3-5 years old, where they appear to daydream without losing consciousness.
240
What is a tonic-clonic seizure?
Also known as grand mal, it involves loss of consciousness, rapid muscle contractions, and relaxation.
241
What are common causes of new onset seizures?
High fevers in small kids, head trauma, hypoglycemia, hyponatremia, and infections like meningitis.
242
What is the treatment for hypoglycemia-induced seizures?
Administer dextrose (glucose) to reverse the condition quickly.
243
What is the pathophysiology of seizures?
A result of a shift in the normal balance of excitation and inhibition within the CNS, with too much excitation (glutamate) and too little inhibition (GABA).
244
What should be noted during a physical exam of a patient having a seizure?
Signs such as bitten tongue, incontinence, and postictal period.
245
What is epilepsy?
Recurrent unprovoked seizures.
246
What are characteristic changes that accompany seizures in epilepsy?
Characteristic electroencephalographic changes.
247
What are some symptoms (SX) of epilepsy?
Presence of an aura, automatisms (chewing, gestures, scratching, fumbling), loss of awareness and responsiveness, aggressive or vocal outbursts, prolonged confusion.
248
What should be considered right after a seizure?
Altered mental status, sleepiness, incontinence, oral injury.
249
Who should all adults with a new onset seizure see?
A specialist (neurologist, preferably an epileptologist).
250
What is the criteria for diagnosing epilepsy?
2 or more seizures more than 24 hours apart (unprovoked).
251
What tests are commonly performed for epilepsy diagnosis?
1. Electroencephalogram (usually with sleep deprivation)
2. MRI.
252
What studies may be included before starting antiepileptic medications?
Liver function tests, CBC, electrolyte levels, albumin levels.
253
When should anticonvulsant blood levels be assessed?
To determine compliance and in patients with breakthrough seizures, suspected toxicity, and drug interactions.
254
What may prolactin levels help differentiate?
Seizures from pseudoseizures.
## Footnote
If you pick up their arm and drop it, and it hits their face, it is a real seizure.
255
What are non-pharmacologic treatments for epilepsy?
Avoidance of triggers (sleep deprivation, caffeine, fever, alcohol).
256
What are first-line drugs for focal seizures?
Carbamazepine/Oxcarbazepine, Lamotrigine, Phenytoin.
257
What is the first-line drug for absence seizures?
Ethosuximide.
258
What are first-line drugs for tonic-clonic seizures?
Lamictal, Levetiracetam.
259
What is important to consider regarding epilepsy medications?
They can be teratogenic, especially in relation to childbearing plans.
260
What is Status Epilepticus?
A dangerous type of seizure that lasts >5 minutes, or multiple seizures in a row with incomplete recovery in between.
261
What is the first line treatment for Status Epilepticus?
IV diazepam, available in rectal suppositories (can also use lorazepam). Larger doses of benzodiazepines may be needed.
262
What is the second line treatment for Status Epilepticus?
Fosphenytoin or phenytoin.
263
What is the third line treatment for Status Epilepticus?
Barbiturates.
264
What is the fourth line treatment for refractory Status Epilepticus?
Propofol, an anesthesia drug that slows brain activity.
265
What is included in the seizure workup?
IV dextrose/Diazepam, history, lab work, and medications to determine the cause.
266
What is meningitis?
Inflammation of the leptomeninges (inner layers of meninges), including the arachnoid mater and pia mater.
267
Where is the CSF located in relation to the meninges?
The CSF is between the arachnoid and pia mater in the subarachnoid space.
268
What are common triggers for meningitis?
Diseases like lupus, reactions to intrathecal therapy, and infections (most common).
269
What is direct spread in the context of meningitis?
Spread from overlying skin infections, defects like spina bifida or skull fractures, and from the sinuses or mastoiditis.
270
What is hematogenous spread in meningitis?
A pathogen crosses the blood-brain barrier.
271
What are the most common bacterial causes of meningitis in 0-90 days?
Group B strep (agalactiae).
272
What are the most common bacterial causes of meningitis in 3 months to 10 years?
Streptococcus pneumoniae.
273
What are the most common bacterial causes of meningitis in 10 to 19 years?
Neisseria meningitides.
274
What are the most common bacterial causes of meningitis in 19 to 50 years?
Streptococcus pneumoniae.
275
What are the most common bacterial causes of meningitis in patients over 50 years?
Streptococcus pneumoniae and Listeria monocytogenes.
276
What bacterial cause of meningitis is associated with neurosurgery?
Staphylococcus aureus.
277
What viral causes are associated with meningitis in 0-90 days?
Herpes Simplex, most likely from the mother, and enteroviruses (coxsackie virus + many others).
278
What are common viral causes of meningitis?
Arboviruses (arthropod borne, e.g., West Nile) and influenza (rare, mostly in children).
279
What are the fungal causes of meningitis?
Rare, usually occurs in immunocompromised patients, including Cryptococcus, histoplasmosis, and candida (very premature, low birth weight babies).
280
What has caused a decrease in bacterial meningitis in pediatric patients?
The HIB vaccine has led to a decrease in bacterial meningitis in pediatric patients.
281
What vaccine has decreased the incidence of bacterial meningitis in adults over 65?
The pneumococcal vaccine has decreased the incidence in adults over 65.
282
What is the typical onset and progression of bacterial meningitis?
Bacterial meningitis has an insidious onset with rapid progression.
283
What are the most common organisms causing bacterial meningitis?
80% of cases are caused by Streptococcus pneumoniae and Neisseria meningitidis.
284
What are other organisms that can cause bacterial meningitis?
Other organisms include Listeria monocytogenes and staphylococci.
285
What percentage of bacterial meningitis cases are due to gram-negative bacilli?
Less than 10% of cases are due to gram-negative bacilli.
286
What are some examples of gram-negative bacilli that can cause bacterial meningitis?
Examples include Escherichia coli, Klebsiella, Enterobacter, and Pseudomonas aeruginosa.
287
Why does rapid growth occur in the CSF during bacterial meningitis?
Rapid growth occurs because the blood-brain barrier blocks entry of immunoglobulins and complement.
288
What are common symptoms of bacterial meningitis?
Symptoms include altered mental status, fever, headache, neck stiffness, lethargy, nausea and vomiting.
289
What specific rash is associated with meningococcal meningitis?
A petechial rash is associated with meningococcal meningitis.
290
What are some signs of meningeal irritation?
Signs include nuchal rigidity, Kernig's sign, and Brudzinski's sign.
291
What are some additional signs of bacterial meningitis in infants?
Signs include poor feeding, bulging fontanelle, petechial or purpuric rash, and shock.
292
What is the most important diagnostic test for bacterial meningitis?
Blood cultures and CSF samples are the most important diagnostic tests.
293
When should a CT scan be performed prior to a lumbar puncture?
A CT scan should be performed if the patient is immunocompromised or has a history of CNS disease.
294
What is the normal intracranial pressure?
Normal intracranial pressure is 20 mm Hg.
295
What happens if there is an increase in one of the components of the cranium?
An increase causes increased pressure in the cranium, and a lumbar puncture is not recommended.
296
What is the gold standard to measure intracranial pressure?
Pressure waveform is the gold standard to measure intracranial pressure.
297
What is the initial treatment for bacterial meningitis?
Initial treatment is likely to be empiric and broad.
298
What antibiotics are used for immunocompetent children and adults under 55 with bacterial meningitis?
Cefotaxime, ceftriaxone, or cefepime plus vancomycin are used.
299
What additional medication is given empirically in bacterial meningitis treatment?
Dexamethasone is given to reduce the risk of hearing loss and mortality.
300
What is recommended for fluid and electrolyte management in bacterial meningitis?
Careful management of fluid and electrolytes is recommended.
301
What vaccination is recommended for 11 and 12-year-olds?
MenACWY vaccine is recommended with a booster at age 16.
302
Who should receive the MenACWY vaccine?
Adults who are immunocompromised, microbiologists, or traveling to endemic areas should receive it.
303
What is the prophylactic treatment for close contacts of bacterial meningitis patients?
Rifampin for all ages or Ciprofloxacin for adults only.
304
What is the most common cause of Viral Meningitis?
The most common cause (by far) is enterovirus.
305
What are the specific types of enteroviruses associated with Viral Meningitis?
Coxsackie (hand, foot, and mouth) and Echovirus.
306
What are other causes of Viral Meningitis?
Other causes include herpes, mumps, and measles.
307
What are common symptoms of Viral Meningitis?
Respiratory tract symptoms.
308
What are characteristic symptoms of meningitis in adults?
Photophobia, fever > 38 degrees C (100.4 degrees F), and neck stiffness.
309
How may neonates present with Viral Meningitis?
Irritability, lethargy, and bulging fontanelle.
310
How do adults typically present compared to children with Viral Meningitis?
Adults tend to be sicker than kids.
311
What skin findings are associated with Coxsackievirus and Echovirus infection?
Look for maculopapular, nonpruritic rash on face and trunk.
312
What HEENT findings may indicate meningitis caused by Coxsackievirus A?
Presence of painful vesicles on posterior oropharynx.
313
What are the neuro signs associated with Viral Meningitis?
Meningeal signs and bulging fontanelles.
314
What is the diagnostic procedure for Viral Meningitis?
Lumbar puncture (LP) for cell counts, glucose, gram stain, culture, and protein.
315
What is the treatment approach for Viral Meningitis?
Empiric antibiotics if no clear distinction between bacterial and aseptic meningitis, supportive care including hydration and analgesics.
316
Is antiviral therapy available for most viral causes of meningitis?
Antiviral therapy is NOT available for most viral causes.
317
What antiviral treatment is available for herpes virus infections?
Acyclovir.
318
What adjunctive treatment may be used with Viral Meningitis?
+/- dexamethasone.
319
What is Fungal Meningitis and its common cause in the United States?
Fungal Meningitis is rare in the United States, commonly caused by Cryptococcus neoformans.
## Footnote
Typically found in soil, on decaying wood, in tree hollows, or in bird droppings.
320
What is the treatment for Fungal Meningitis caused by Cryptococcus neoformans?
The treatment is Amphotericin B.
321
What is Histoplasmosis-Fungal Meningitis and its reservoir?
Histoplasmosis-Fungal Meningitis has a reservoir in soil, particularly when heavily contaminated with bird or bat droppings.
## Footnote
Endemic areas include the central and eastern United States, particularly around the Ohio and Mississippi River Valleys.
322
What is the treatment for Histoplasmosis-Fungal Meningitis?
The treatment is Amphotericin B.
323
What is Blastomyces Fungal Meningitis and its reservoir?
Blastomyces Fungal Meningitis has a reservoir in soil and decaying organic matter such as wood or leaves.
## Footnote
Endemic areas in the US include the midwestern, south-central, and southeastern states, particularly around the Ohio and Mississippi River valleys.
324
What is the treatment for Blastomyces Fungal Meningitis?
The treatment is Amphotericin B.
325
What is Coccidioidomycosis and where is it endemic?
Coccidioidomycosis is a fungal pneumonia endemic in Arizona and the San Joaquin Valley in California.
326
What is the treatment for Coccidioidomycosis?
The treatment is Fluconazole.
327
What is a brain abscess?
Purulent material in the brain parenchyma.
328
What is the common site of infection for brain abscesses?
Head and neck.
329
How does a brain abscess typically spread?
Hematogenous spread from an endovascular source, such as endocarditis.
330
How long can symptoms of a brain abscess take to manifest?
Days to weeks.
331
What imaging technique is preferred for diagnosing a brain abscess?
MRI due to higher sensitivity.
332
What will a CT scan show in cases of brain abscess?
Ring enhanced lesions that will go away after infection.
333
What is the treatment for a brain abscess?
Antibiotics (Ceftriaxone + Metronidazole or Vancomycin) + neurosurgery.
334
How long should antibiotics be continued for a brain abscess?
6-8 weeks of IV antibiotics.
335
What can be given to reduce inflammation in a brain abscess?
Dexamethasone.
336
What is a minimally invasive procedure for brain abscess treatment?
Stereotactic neurosurgical aspiration.
337
What complications can arise from a brain abscess?
Seizures, meningitis, increased intracranial pressure, and brain herniation.
338
What is encephalitis?
Inflammation of the brain parenchyma caused by infection or a primary autoimmune process.
339
What is the most common virus associated with encephalitis?
HSV-1.
340
What diagnostic tests are helpful for encephalitis?
Antibody/PCR.
341
What imaging is preferred for diagnosing encephalitis?
MRI.
342
What is the treatment for encephalitis?
Monitoring of ICP, fluid restriction, and avoidance of hypotonic intravenous solutions.
343
How should seizures in encephalitis be treated?
With standard anticonvulsant regimens, and prophylactic therapy should be considered.
344
What medication can be used for HSV in encephalitis?
Acyclovir.
345
What is mass effect in the context of brain conditions?
Some encroachment upon the ventricles of the brain.
346
What is an epidural hematoma (EDH)?
A hematoma that arises in the potential space between the dura and the skull, usually caused by head trauma.
347
What is a common symptom of an epidural hematoma?
Patients may have a 'lucid interval' before losing consciousness.
348
What is a key diagnostic feature of an epidural hematoma on CT?
Lens-shaped bleed (biconvex pattern).
349
What is contraindicated in cases of suspected epidural hematoma?
Lumbar puncture.
350
What is the mainstay of surgical treatment for an epidural hematoma?
Craniotomy and hematoma evacuation.
351
What is the treatment for mild epidural hematoma?
Monitoring with serial imaging.
352
How can intracranial pressure (ICP) be managed?
Elevate head of bed, hyperventilation, and osmotic diuresis with intravenous mannitol.
353
What is the Cushing reflex?
Hypertension, bradycardia, and respiratory depression/irregularity.
354
What is a Subdural Hematoma (SDH)?
SDH forms between the dura and the arachnoid membranes.
355
What are common causes of Subdural Hematoma?
Head trauma, especially in the elderly, alcoholics, babies, and people on anticoagulants.
356
What causes Acute Subdural Hematoma?
Tearing of the bridging veins that drain from the surface of the brain to the dural sinuses.
357
When do symptoms of Acute Subdural Hematoma typically present?
Symptoms present one to two days after onset.
358
What are symptoms of Acute Subdural Hematoma?
Symptoms include headache, vomiting, anisocoria, dysphagia, cranial nerve palsies, nuchal rigidity, and ataxia.
359
When do symptoms of Subacute Subdural Hematoma typically present?
Symptoms present 3 to 14 days after onset.
360
When do symptoms of Chronic Subdural Hematoma typically present?
Symptoms present 15 or more days after onset.
361
What are global deficits associated with Chronic Subdural Hematoma?
Insidious onset of headaches, light-headedness, cognitive impairment, apathy, somnolence, and occasionally seizures.
362
How is Acute Subdural Hematoma diagnosed?
It is readily visualized on head CT as a high-density crescent.
363
How do Subacute and Chronic Subdural Hematomas appear on imaging?
They appear as isodense hypodense crescent-shaped lesions.
364
What is the treatment for Subdural Hematoma?
Operative or non-operative management, and reverse anticoagulation.
365
What is a Subarachnoid Hematoma (SAH)?
Most cases are caused by rupture of an intracranial aneurysm.
366
What are other causes of Subarachnoid Hematoma?
Trauma, vascular malformations, cerebral venous thrombosis, cocaine use, and bleeding disorders.
367
What are the risk factors for Subarachnoid Hematoma?
Cigarette smoking, hypertension, genetic factors, alcohol, sympathomimetic drugs, and antithrombotic therapy.
368
What is a key symptom of Subarachnoid Hematoma?
THUNDERCLAP HEADACHE: sudden-onset, severe headache described as the 'worst headache of my life.'
369
How is Subarachnoid Hematoma diagnosed?
CT scan and lumbar puncture if suspicion remains despite normal CT.
370
What does lumbar puncture reveal in cases of SAH?
It shows blood and visual inspection for xanthochromia.
371
What is the treatment for Subarachnoid Hematoma?
Blood pressure control, correcting coagulopathy, and preventing rebleeding by early repair of the aneurysm.
372
What is Intracerebral Hemorrhage (ICH)?
The second most common cause of stroke, primarily caused by bleeding from arteries in the brain parenchyma.
373
What is the greatest risk factor for Intracerebral Hemorrhage?
Hypertension.
374
How is Intracerebral Hemorrhage diagnosed?
Neuroimaging with CT or MRI is mandatory.
375
What are the imaging markers for increased risk of hemorrhage expansion in ICH?
The spot sign and swirl sign.
376
What is the treatment for Intracerebral Hemorrhage?
Medical emergency requiring BP control, reversing anticoagulants, ICP monitoring, and possible surgical intervention.
377
What is the treatment for cerebellar hemorrhage?
Surgical removal of hemorrhage with cerebellar decompression for hemorrhages greater than 3 cm.
378
What is the treatment for supratentorial hemorrhage?
Surgery is reserved for life-threatening mass effect.
379
What is the treatment for intraventricular hemorrhage?
Close monitoring and ventriculostomy if developing hydrocephalus.
380
What is Traumatic Brain Injury (TBI)?
Brain function impairment resulting from external force.
381
What age groups have the highest rates of TBI?
Ages 0-4, 15-24, and age > 65.
382
How is TBI severity assessed?
Using the Glasgow Severity Scoring Scale.
383
Glascow Scoring Scale
Clinical Severity Scoring:Glasgow Coma Scale (GCS)
Mild (13-15)
Moderate (9-12)
Severe (<8)
384
What are the two categories of disease in Traumatic Brain Injury?
1. Primary brain injury: Occurs at the time of trauma
2. Secondary brain injury: Occurs after the initial injury
385
What is the mechanism of injury (MOI) for primary brain injury?
Direct impact, rapid acceleration/deceleration, penetrating injury (ex: gunshot wound), blast waves (military)
386
What are the types of injuries resulting from primary brain injury?
Diffuse Axonal Injury, Cerebral contusions, Hematomas (Epidural Hematoma, Subdural Hematoma, Subarachnoid Hemorrhage, Intraventricular Hemorrhage)
387
What is secondary brain injury?
A series or cascade of molecular injury mechanisms initiated by the initial trauma, potentially leading to brain edema and/or brain herniation.
388
What are examples of secondary brain injury mechanisms?
Hypoxia/ischemia, increased ICP, hydrocephalus, infection, tissue injury, and chemical reactions (toxins)
389
What is diffuse axonal injury (DAI)?
Associated with sudden deceleration injuries involving stretching, shearing, tearing of nerve fibers and axonal damage.
390
What are the typical clinical presentations of diffuse axonal injury?
Profound coma without elevated ICP and poor neuro prognosis. Best seen on MRI.
391
What is a focal cerebral contusion?
The most commonly seen lesions, described as a big bruise, typically in basal frontal and temporal areas.
392
What symptoms should be noted in traumatic brain injury?
Fractures, skull fracture, post-traumatic seizures, scalp hematomas.
393
What does raccoon eyes indicate?
Bruising around the eyes that indicates basilar skull fracture.
394
What is Battle sign?
Bruising behind the ears is a sign of basilar skull fracture.
395
What is hemotympanum?
Blood behind the tympanic membrane indicates basilar skull fracture.
396
How does Epidural Hematoma, Subdural Hematoma, Subarachinoid Hematoma, and Intraventricular Hematoma look like on imaging?
397
Decorticate posture and Decerebrate posture
Decorticate posture: cerebral hemisphere injury.
Decerebrate posture: brainstem injury
398
What are the two ways to calculate risk for head CT in traumatic brain injury?
1. PECARN defines low risk clinical decision rules for pediatric patients. 2. Canadian Head CT rules for adults.
399
What are the exclusion criteria for head CT in adults?
Answer yes to any of these: Under 16, on blood thinners, seizure after injury.
400
What are the high/medium risk criteria indicating a CT should be done?
GCS < 15 at 2 hours post injury, suspected open or depressed skull fracture, any sign of basilar skull fracture, > 2 episodes of vomiting, age over 65 years, retrograde amnesia > 30 mins, 'dangerous' mechanism (e.g., fall from 3-6 feet, ejected from moving vehicle).
401
What is the initial treatment for traumatic brain injury?
ABCs, Mannitol to lower ICP, treat seizures if needed, emergency craniotomy or burr holes for decompression.
402
What defines a concussion?
Concussion is a GCS score of 13 to 15 assessed 30 minutes after injury, with no demonstrable injury on standard neuroimaging.
403
What are the symptoms of concussion?
Headache, inattentiveness, slow or incoherent speech, dizziness.
404
What is the treatment protocol following a concussion?
Physical and cognitive rest for 24-48 hours, followed by gradual activity increase. Use sport-specific helmets.
405
What is Post Concussive Syndrome?
A symptom complex following TBI that includes headache, dizziness, neuropsychiatric symptoms, and cognitive impairment.
406
What are the common symptoms of Post Concussive Syndrome?
Sleep disturbance, personality change, irritability, noise intolerance, impaired memory.
407
What is the treatment for Post Concussive Syndrome?
Cognitive or physical rest, headache management with Amitriptyline.
408
What role does alcohol play in spinal cord injuries?
Alcohol is involved in at least 25 percent of spinal cord injuries.
409
What is the initial management for spinal cord injury?
ABCs and immobilization. Athletic headgear should be left on.
410
What imaging is performed for suspected spinal cord injury?
C-spine imaging is often performed; CT is more sensitive for bone damage, MRI shows spinal cord damage.
411
What defines complete spinal cord injury?
Complete loss of motor and sensory function below the spinal cord injury.
412
What is Brown-Sequard Syndrome?
A syndrome resulting from penetrating trauma, characterized by contralateral loss of pain, temperature, light touch, and ipsilateral loss of motor function, vibration, proprioception.
413
What is Central Cord Syndrome?
Usually results from hyperextension injury, with greater motor impairment in the upper body.
414
What are the components of the spinal cord structure?
Gray matter contains nerve cell bodies; white matter contains bundles of myelinated axons.
415
What do ascending and descending pathways do in the spinal cord?
Ascending pathways carry sensory information to the brain; descending pathways carry motor information from the brain.
416
What is the population affected by Epidural Hematoma?
Adolescents and adults.
417
What is the vascular source of Epidural Hematoma?
Middle meningeal artery.
418
What is the CT appearance of Epidural Hematoma?
Lens-shaped bleed.
419
What is a notable characteristic of Epidural Hematoma?
"Lucid interval"; LP contraindicated.
420
What is the population affected by Subdural Hematoma?
Elderly, alcoholics, babies, and people on anticoagulants.
421
What is the vascular source of Subdural Hematoma?
Venous bleed of bridging veins.
422
What is the CT appearance of Subdural Hematoma?
Crescent shaped.
423
What are the types of Subdural Hematoma?
Present as acute, subacute, or chronic.
424
What is the population affected by Subarachnoid Hemorrhage?
50-55 years.
425
What is the vascular source of Subarachnoid Hemorrhage?
Arterial and venous malformations.
426
What is the CT appearance of Subarachnoid Hemorrhage?
Anywhere CSF is present (especially in the ventricles).
427
What is a notable symptom of Subarachnoid Hemorrhage?
Thunderclap headache.
## Footnote
Repair the aneurysm with surgical clipping or endovascular coiling.
428
What is the population affected by Intracerebral Hemorrhage?
Adults.
429
What is the vascular source of Intracerebral Hemorrhage?
Arteries of the brain parenchyma.
430
What is the CT appearance of Intracerebral Hemorrhage?
Spot and swirl.
431
What are the risk factors for Intracerebral Hemorrhage?
HTN; this condition has a high mortality rate.
