!Neuropharmacology Clin Med Flashcards
(371 cards)
1
Q
What is a primary head ache
A
Benign disorder
2
Q
What is a secondary headache
A
Sign of organic disease
3
Q
What are the types of primary headaches
A
Migraine(with or without aura)
- chronic migraine
- tension type
- cluster
- post traumatic
- drug rebound
- trigeminal neuralgia
4
Q
Headache history
A
How many types
Frequency
Pain
Prodrome (changes in energy levels, mood appetite, fatigue, muscle aches aura)
Associated symptoms-nausea, vomiting, anorexia, photophobia, photophobia, diarrhea, dizzy, behavior (retreat to dark, paces, rocks)
Previous medications tried
Medical/surgical history
Family history
5
Q
Head ache exam
A
General examination (vitals, cardiac, extracranial, ROM C spine)
Neuro exam
6
Q
Worrisome signs with headache
A
Worst HA
Onset after 50
Atypical for patent
Abrupt onset
Subacute with progressive worsening
Drowsi, confusion, memory
Weakness, ataxia, loss of coordination
- paresthesia/sensory loss/analysis
- abnormal medical or neuro exam
7
Q
Diagnostic evaluation HA
A
Lab test, neurodiagnostic tests
8
Q
What labs run with HA
A
CT, MRI/MRA, EEG, L.P. Arteriogram
-dental ENT allergy
9
Q
As a general rule, HA patient should have a one-time, thurought neuro study
A
CT head with and without MRI of head
10
Q
What do if have worrisome history or abnormal exam
A
Urgent imaging study and perhaps even and LP and arteriogram
11
Q
CT can miss _% of subarachnoid hemorrhages and an LP may be needed if CT is normal
A
5-10%
12
Q
What is difference between common and classic migraine
A
Common-no aura
Classic-aura
13
Q
Intensity of common migraine
A
Moderate to severe
14
Q
Disability common migraine
A
Inhibits or prohibits daily activities, pain aggravated by activity
15
Q
Age onset common migraine
A
Late teens to early 20s
Prevalence peaks 35-40
16
Q
Female:male ration for common migraine
A
3:1
17
Q
Frequency common migraine
A
1-4 attacks per month (occasional) but 14 days or fewer per month
18
Q
Duration common migraine
A
4 to 72 hours
Usually 12-24
19
Q
Location common migraine
A
Unilateral or bilateral
20
Q
Description common migraine
A
Throbbing/sharp/pressure
21
Q
Prodrome common migraine
A
Mood changes, myalgia, food cravings, sluggishness, excessive yawning
22
Q
Post drone common migraine
A
Fatigue, irritability, fog
23
Q
Behavior common migraine
A
Retreat to dark, quiet room
24
Q
Aura common migraine
A
None
25
_% of migraine sufferers don’t get aura
80-90
26
Associated symptoms of common migraine
Nausea, vomiting, photophobia, photophobia
| Uncommon-diarrhea, conjunctival injection, stuffy nose, lacrimation, miosis, ptosis
27
Classic migraine
Aura (flashing lights or zig zag lines preceded migraine headache)
Aura lasts 15-30 minutes (scintillation, scotoma-often hemianopic)-but can be anything neurological
28
Chronic migrain
15 or more days per month, headache lasting 4 hours or longer, for a period of at least 3 months, not attributable to another disease
29
What causes migraines
Neurogenic inflammation
-trigeminal nerve becomes activated , releasing neuropeptides, causing painful neurogenic inflammation within the meninges, with subsequent effect on the dural vasculature (vasodilation, plasma protein extravasation, and mast cell degranulation)
30
Tension headache intensity
Mild to moderate
31
Tension HA disability
May inhibit but does not prohibit daily activities
32
Tension HA age of onset
Generally pear 20-40 years
33
Female to ace ration tension HA
3:2
34
Frequency tension HA episodic type
<15 days a month
35
Frequency tension HA chronic type
>15 days a month?/ analgesic rebound HA, consider chronic migraine if intermittent migraines also present
36
Duration tension HA episodic
Several hours
37
Duration tensionHA chronic
All day, waxing and waning
38
Location tension HA
Bifrontal, bioccipital, neck, shoulders, band like
39
Description tension HA
Dull, aching, squeezing, pressure
40
Aura with tension HA
No
41
Behavior and tension HA
Not affected
42
Cluster HA intensity
Severe excruciating
43
Disability cluster HA
Prohibits daily activities
44
Age onset cluster HA
20s-50s
45
Female to male ration cluster HA
1:6
46
Cluster headache has recent association with __ _ _-
Obstructive sleep apnea
47
Cluster HA frequency episodic
1 or more a day for 6-8 weeks
48
Cluste HA frequency chronic
Several attacks per week without remission
49
Duration cluster HA
30 min-2 hr
50
Location cluster HA
100% unilateral, generally orbitotemporal
51
Pain of cluster HA
Non throbbing, excruciating sharp, boring, penetrating
52
Prodrome cluster ha
May include brief mild burning in ipsilateral inner canthus or internal nares
53
Aura cluster ha
No aura
54
Behavior cluster HA
Frenetic, pacing, rocking
55
Associated symptoms cluster HA
Ipsilateral ptosis, miosis, conjunctival injection, lacrimation, stuffed or runny nose
56
What triggers HA
Hormones, diet, stress, sensory stimuli
57
Hormones that trigger HA
Menses, ovulation, HRT, OC
58
Diet hat triggers HA
Alcohol , chocolate, aged cheese, MSG, aspartame, caffeine, nuts, nitrates/nitrites, citrus fruits, other
59
Changes that trigger migraine
Weather, seasons, travel, altitude, schedule, sleep patter, diet, skipping meals
60
Stress for HA trigger
Let down periods, intense activity, major life change/stress
61
Sensory stimuli of HA triggers
Bright or flickering lights odors
62
Acute treatment of migraine
OTC analgesics
NSAIDS-naproxen, ketorolac, diclofenac, isometheptene (midbrin), butalbital (fiorinal, fioricet)
Opoids-Demerol, morphine, codeine, oxycodone, hydrocodone
DHE nasal spray
Tristan’s
63
What are Triptans
5HT1 agonist
64
Name the triptans
```
Sumatriptan
Zolmitriptan
Naratriptan
Rizatriptan
Almotriptan
Frovitriptan
Sumatriptan
Sumatriptan/long acting naproxen (treximet)
```
65
Triptans contraindicated in
Documented or strong risk factors for ischemic heart disease, other cardiovascular, cerebrovasculat or peripheral vascular disease, Raynaud syndrome, uncontrolled HTN, hemiplegic r basilar migraine, severe renal or hepatic impairment, use within 34 hours of tax with ergotamines, MAOIS or other 5HT1 agonists
66
Naratriptan dose
3.5 mg-one tablet at onset, may repeat 1 in 3 hr (max 10 mg in 24 hours)
67
Onset of action naratriptan
60 min
68
Benefits of naratriptan
Longest half life and fewest side effects
69
Contraindication for naratriptan
Patients with severe hepatic or renal impairment
70
Zolmitriptan dose
2.5,5 mg one at tablet onset HA may repeat 1 in 2 hours
Max 10 mg 24 hours
71
Onset action zolmitriptan
30-60 min
72
__ dose of solmitriptan recommended in patients with ___ impairment
Low hepatic
73
Sumatriptan dose
Up to 100 mg as a single dose and may repeat in 2 hours
Max 200 mg in 24
Onset 30-60min
74
Nasal spray sumatriptan
One spray at onset repeat 2 hours
Max 12 mg in 24 hours
Onset 10 min
75
Sumatriptan injection
One SQ at onset of MA, may repeat in 1 hr
Max 12 mg in 24 hours
Onset 10 min
76
Rizatriptan dose
One 5 or 10 mg tab at onset repeat in 24 hours
Max dose 20 mg in 24 hours
(Use 5 mg in patients on propranolol for max does of 10 in 24)
77
Almotriptan dose
12.5 mg tablets one at onset repeat 24 hours
Max 25 mg in 24 hours
78
Frovatriptan
2.5 tablet at onset repeat 1x in 24 hours
Max 7.5 in 24 hours
79
Frovatriptan
2. 5 onset repeat two hours
| 7. 5 mg in 34 hours
80
If triptans doesn’t work
Try another , consider nasal or injectable if needed
81
What is the DHA protocol
Metoclopromide or prochlopereazine 10 mg IV over 60 sec. wait 5 min to allow distribution
Give DHE .5 mg IV over 60 sec wait 3-5 min
May repeat .5 mg IV if no relief every 8 hours for short term use
82
Contraindications DHE
Same as triptans
83
Side effects HE
Chest pressure, anxiety, speeding or dissociation of thoughts, nausea
84
If nausea/vomiting are a major feature of migraine, consider using a ____
Antimemtic like metoclopramide, prochloperazine
85
If insomnia is a major feature of migraine, consider a ____ or ___ to help patient sleep off migraine
Sedative-diazepam, temazepam
Tranquilizer-thorazine
86
A __ __ can sometimes be used to break the cycle of a prolonged migraine or several weeks of frequent migraines
Prednisone taper
87
What should you do if patient has one or more migraines a week
Preventative
88
Antidepressants to prevent migraines
TCA (amitriptyline, nortriptyline)
SSRI (fluoxetine, sertaline, escitalopram)
MAOI (phenelzine)
Beta blockers (propranolol)
Calcium channel blockers (verapamil)
Anticonvulsants (topiramate, valproic acid, gabapentin)
Ergot alkaloids (ergotomine+phenobarbital)
NSAIDS (ASA, naproxen)
Muscle relaxants (tizanidine)
Methysergide (sansert)
89
Botox injection
For chronic migraine
155 units into 31 sisters repeated 3 months
Need multiple treatments over 9-12 months to work
minimal side effects
90
Non prescription treatment of migraine
Exercise, stop smoking, HA education, riboflavin, mg, biofeedback/relaxation/stress management
91
What is one of the best preventative treatments of migraine and tension type HA
Stress management/relaxation/biofeedback
92
Acute treat of tension headache
OTC analgesics
NSAIDS
Opoids
Midbrain
93
Acute treat of tension HA
OTC analgesics
NSAIDs
Opoids
Midrin
94
Preventative treat for tension HA
```
Antidepressents
-Tca, SSRI, MAOI
Muscle relaxant
Anticonvulsants
BOTOX injection
Ergot alkaloids(DHE sometimes used to break cycle of chronic HA
```
95
Acute tc of cluster headache
DHE 1 mg IM or ergotamine 3 mg SL
Lidocaine 4% intranasal
Narcotics
Oxygen 6Lmin by mask
Sumatriptan 6 mg
96
Preventative treat for cluster headache
```
Calcium channel blocker
Anticonvulsant
Lithium
Indomethacin
Prednisone 10-14 days
Ergotamine tartare
```
97
Trigeminal neuralgia
Excruciating sharp shooting electrical quality pain occurring in paroxysms in one or more distributions of the trigeminal nerve often frequent throughout the day.
98
Treat trigeminal neuralgia
Carbamazepine or oxcarbamazepine
Other anticonvulsants or surgery
99
Trigeminal autonomic cephalgias TAC
Group of headache disorders characterized by unilateral trigeminal distribution pain that occurs in association with prominent ipsilateral cranial autonomic features
100
What does TAC include
```
Cluster HA
Paroxysmal hemicrania
Hemicrania continua
SUNCT syndrome
SUNA syndrome
```
101
SUNCT syndrome
Short lasting, unilateral, neuralgiform headache attacks with conjunctival injection and tearing
102
Symptoms SUNCT
Excruciating, burning, stabbing electrical HA in periorbital area lasting seconds to a few minutes, occurring frequently throughout the day
Onset over 50 in men
103
Treat SUNCT
Anticonvulsants
| LAMOTRIGINE
104
Paroxysmal hemicrania
Very similar to cluster headache (unilateral, periorbital, severe, excruciating, often with lacrimation, conjunctival irritation) but shorter duration (few minutes) and increased frequency (over 5 a day)
105
Treat paroxysmal hemicrania
Indomethacin
106
MS
Disorder of the brain and spinal cord characterized by a tendency for periods of increasing and decreasing symptoms and signs (exacerbation and remissions), which result from loss of nerve tract insulation (myelin) at multiple sites in the CNS
107
Common presentation of MS
```
Paresthesias
Gait (transverse myelitis)
Weakness
Visual loss (optic neuritis)
Urinary difficulty
Dysarthria
Hemiparesis
```
108
Four types of MS
```
Relapsing remitting (45-50%)
Secondary progressive (20-25%)
Primary progressive (15-20%)
Benign (20-15%
```
109
What is secondary progressive MS
Begin their disease process in the relapsing remitting category-includes some patients that still have occasional relapses (relapsing progressive
110
When is MS diagnosed
20s-30s
111
Characterization MS
Exacerbation and remission
112
Diagnose MS
No single test, multiple studies can help
113
Cause of MS
Unknown
| Genetic, immune to CNS myelin triggers(virus and stuff)
114
Women or men MS
Women, but women more favorable course
115
With MS early onset is a more __ prognosis
Favorable
116
Tropical or temporal zones MS
Temperate
117
How diagnose MS
MRI of head, and C T spine
-ovoid lesions on T2W1 in periventricular white matter and in spinal cord
Multimodality evoked potentials (SSEPs, VEP, BAER
- LP
- oligoclonal bands and/or increased IgG index/synthesis rate are the typical findings in MS
118
Drugs for MS maintence
```
Avonex, rebif
Betaseron
Cop a one
Tysabri
Gilenya
Tecfidera
Lemtrada
Zinbryta
Ocrevus
```
119
What is used t treat primary progressive MS in addition to relapsing forms of the disease
Ocrevus
120
How treat acute exacerbation in MS
High dose corticosteroids (methylprednisone-1 gram IV daily for 305 days followed by oral prednisone taper)-this reduces length of exacerbation but is not thought to change the voverall outcome of it
ACTH IVIg can be used on occasion, particularly in patients who do not tolerate traditional steroid treatment
121
CLinically Isolated SYndrome
A disease course of MS that can be monofocal or multifocal
122
Monofocal episode of clinically isolated syndrome
Person experiences a single neurologic sign or symptom that’s caused by a single lesion (optic neuritis in one eye)
123
Multifocal episode of clinically isolated syndrome/acute disseminated encephalomyelitis
More than one sign or symptom caused by lesions in more than one place (optic neuritis in one eye plus hemiparesis)
124
When do CIS patients have a high risk of developing MS
Multiple demyelinating lesions on MRI,
60-80% chance of developing in several years
125
When do CIS patients have a low risk of developing MS
Do not have multiple demyelinating lesions on MRI, have about a 20% chance of developing MS within several years
126
What disease may mimic MS
```
Autoimmune disease-SLE with cerebritis or CNS vasculitis or polyarteritis nodosa with transverse myelitis
-Devics disease (neuromyelitis optica)
-b12 defiency
-lymphoma or leukemia within CNS
-spinocerebellum ataxia
-vascular malformations
Infections
Granulomatous disease-sarcoidosis
-metachromatic leukodystrophy, adrenomyeloleukodystrophy
```
127
How manage spasticity of MS
Baclofen, tizanidine, diazepam, carbamazepine, Botox, dantrolene
128
How manage intention tremor
Propranolol, primidone, clonazepam
129
How manage urinary urgency
Oxybutinin
| Destroy LA
130
How manage urinary retention/hesitancy
Bethanechol
131
Howmanage painful dysesthesias
```
Carbamazepine
Oxcarbazepine
Gabapentin
Phenytoin
Baclofen
```
132
How manage fatigue
Amantadine, modafinil, armodafinil, buproprion, methylphenidate, pemoline, exercise
133
Cure for MS
No
134
Devics disease/neuromyelitis optica
Variant of MS, but probably a different entity
Inflammation, demyelination of optic nerves and spinal cord
Spare brain
Yeast for aquaporin 4 antibodies
-
135
How treat devics
Steroids, plasma exchange, followed by immunosuppression (azothiaprine, mycophenolate, mofetil, rituxumab)
136
What is paroxysmal disorders
Episodic!
| -migraines, syncope, dizziness, seizure, transient global amnesia
137
Epilepsy
2 or more unprovoked seizures
4th most common neurological disorder
1/26 ppl will develop
138
Prejudice of epilepsy
Possessed by demons
Contagious
Up until 1965 illegal for epilepsy patients to marry in 17 states
Last state abolish in 1980
Can deny them in restaurants, theaters, and other public places until 1970s
Underemployment
Stopped in 1990 with American Disability act
139
% positive findings for epilepsy on a single EEG
```
All types 40%
Generalized tonic closure 20%
Petit mal (with HV) 90%
```
140
Percent positive for epilepsy (al types) with 3 sleep-deprived EEG is __
85%
141
A normal EEG does not exclude the presence of ___
Epilepsy
142
Minor abnormalities on an EEG do not necessarily indicate a patient will have __
Seizures
143
Partial seizure (on one side of brain)
Simple partial
Complex partial
Secondarily generalized (partial onset)
144
Generalized seizures
```
Absence (petit mal)
Tonic clinic
Myoclonic
Tonic
Clinic
Atonic
Clinic tonic clonic
```
145
Dimple partial seizure
Focal motor or sensory activity, no LOC, lasts seconds, no post octal state
146
Complex partial seizures
Non responsive staring, possible preceding aura, automatism, LOC, lasts 102 min, post-vital state
147
Characteristics of secondary generalized seizures
Bilateral tonic clonic activity, LOC, lasts 1-3 min, post entail state
148
Absence generalized seizures
Non responsive staring, rapid blinking, chewing, clonic hand motions, LOC, lasts 10-30 sec, no post octal state
149
Generalized tonic clonic seizures
Bilateral extension followed by symmetrical jerkingof extremities, LOC, lasts 1-3 min, post-ictal state
150
Generalized atonic seizures
Sudden loss of muscle tone, head drops, or patient collapses, LOC, variable duration, post ictal state
151
Myoclonic generalized seizures
Brief, rapid symmetrical jerking of extremities and/or torso, LOC, lasts < few seconds, minimal post ictal state
152
What can we use to treat partialsecondary generalized seizures
```
Valproic acid
Lamotrigine
Leciteracetam
Zonisamide
Perampanel
```
153
What can we use to treat primary generalized seizures
```
Valproic acid
Lemotrigine
Leviteracetam
Zonisamide
Perampanel
Topiramate
```
154
One single combination of AEDs that has been shown to be synergistic in the treatment of epilepsy (espicially for primary generalized seizures) is __ ___ and ____
Valproic acid and lamotrigine
155
Status epilepticus
Condition characterized by prolonged seizure (generally greater than 10 minutes or repeated seizures without recovery in between
156
Treatment status epilepticus
ABC, IV
History
Labs:accuchek, CBC, chemistry panel, drug levels
Non-contrast CT head
Give benzodiazepine (lorazepam 2-4 mg IV)
-this buys time, but must give longer lasting AAED
-fosphenytoin (18mg/kg) IV (can give IM if no IV access possible) 100mg.min slow rate if BP drops
Phenobarbital-must incubate first, in anticipation for respiratoy depression
Valproic acid 500 mg every 4 hours-total 2000 mg in 24 hours
-lacks amide 200 mg every 12 hours (watch for cardiac conduction abnormalities)
If unsuccessful, try midazolam or propofol continuous IV drop (incubate)
Last resort: pentobarbital coma
In some cases a patient may only respond to one of the oral anticonvulsants (carbamazepine) consider establishing a nasogenic tube for administration
157
General principles in treatment of epilepsy
Try monotherapy
Consider drug interactions -oral contraceptives with carbamazepine
Consider long term side effects-bone loss with carbamazepine of phenytoin
158
All women of child bearing age should be on __ with 1 mg folic acid. This is important for women with epilepsy as many of the AEDs are folate depleting
MV1
159
Pregnant women should avoid __ __
Valproic avid
160
The newer antiepileptic drugs are safer in pregnancy than older ones but the drug of choice for a woman with epilepsy is the drug which best controls her seizures. What are new and old
New-lamotrigine, leviteracetam
Old—phenytoin or valproic acid
161
Syncope
Pallor, sweating, abnormal head sensation, light head, positionally related, slow onset, brief unconsciousness
162
Seizure
Urinary or bowel incontenance, tongue injury, tonic/clonic movements, postictal state
163
Transient global ischemia
Sudden temporary isolated episode of loss of memory (amnesia)
No other neurologic symptoms or signs
Patient knows self and close family/friends, but may not recognize others
Usually lasts a few hours, then resolves
Usually doesn’t recur
164
What are the two types of movement disorders
Bradykinetic
| Hyperkinetic
165
Bradykinetic disorders (a kinetic rigid syndromes)
Most common in Parkinsonism which encompasses many disorders:
- idiopathic Parkinson’s disease
- postencephalitic (Von Economos encephalitis
- toxin induced (manganese, carbon disulfide, CO)
- drug induced (metocolopramide, neuroepileptics like haloperidol, prochloperazine)
- MPTP(meperidine analogue)
166
Idiopathic parkinsons Disease cause
-depletion of dopamine int he nigrostriatal system , disrupting the balance of dopamine and acetylcholine
167
Calincial findings idiopathic Parkinson’s disease
Tremor-resting tremor often unilateral at first pill rolling quality may see mouth or chin tremor
Rigidity0increased resistance to passive movement cogwheel quality
Bradykinesia-slowness of movement ; often difficulty initiating movement
168
Progressive supranuclear palsy
Bradykinesia and rigidity
| Loss of voluntary control of eye movements (vertical gaze)
169
MSA Shy Drager syndrome
Bradykinesia and rigidity
| Pronounced an autonomic dysfunction
170
Cortical basal degeneration
Both cortical and basal ganglionic dysfunction
Bradykinesia and rigidity
May also see cortical sensory loss, apraxia, myoclonus or aphasia
171
Anti parkinsonian medications have little effect on other akinetic rigid syndromes
PSP, MSA, CBD
172
Anti parkinsonian treatment
```
Dopamine agonists (bromocriptine)
Levodopa
COMT inhibitors
Anticholinergics
MAO-B inhibitors
Amantadine
Surgery
```
173
Hyperkinetic movement disorders
Chores , athetosis, dystonia, ballistics, Tic
174
Sydenham’s chorea
In kids as complication of a previous infection with group A hemolytic step . May be arteritis
Characterized by unilateral choreiform movements which when mild can be confused for restless or fidgeting. May also see behavioral changes
175
Treat Sydenham’s chorea
Bed rest and antibiotics
176
Idiopathic torsion dystonia
Characterized by dystonia movements and postures without other signs
May be inherited AD, AR, or X linked
Onset may be childhood or later life, but remains throughout life
177
Idiopathic torsion dystonia
Torticollis, blepharospasm, oromandibular dystonia, arm may be held in hyperpronated position with wrist flexed and fingers extended
Leg may be held in extension, with pronation and inversion of the foot
178
Treat idiopathic torsion dystonia
```
Low doses levodopa
Anticholinergics
Benzodiazepines
Neuroleptic drugs
Baclofen
Carbamazepine
```
179
Focal torsion dystonia
Dystonia confined to focal area
Blepharospasm
Oromandibular dystonia
Spasmodic torticollis
Writers cramp
180
Treat focal torsion dystonia
Botox
181
Wilson’s disease
```
AR copper metabolism dysfunction that produces neurologic and hepatic dysfunction
Chromosome 13(gene ATP7B involved in transportation of copper)
Decreased binding of copper to ceruloplasmin leading to large amounts of free copper deposited into tissues
```
Presents in childhood or young adult life
182
Clinical features Wilson’s disease
Bradykinetic and hyperkinetic features
Resting or postural tremor
Choreiform movements
```
Rigidity
Bradykinesia
Dysarthria, dysphagia
Ataxia
Personality/behavioral changes
Dementia
Psychosis/hallucinations
```
183
Diagnosis Wilson’s
Based on history, exam findings
Increased amounts of copper excretion in 24 hours urine collection
Decreased serum ceruloplasmin level
Kayser fleischer ring on eye exam
184
Treat Wilson
Penicillmaine (a copper chelating agent
Restriction of dietary copper
185
Tic disorders
Single motor tics (blinking, coughing, throat clearing)) often occur as a benign entity
Gilles de la Tourette’s syndrome-chronic multiple motor and vocal tics with onset before the age of 21
186
Gilles de la Tourette’s syndrome
Most cases sporadic
Males
Vocal tics vary in presentation, but can involve barks, hisses, grunts, throat clearing, coughing among others
See-coprolalia (vulgar or obscene speech), echolalia (parroting speech of others), echoproxia (imitation of others movements), palillalia (repetition of words of phrases)
187
Treat Gilles de la tourettes
Clonidine
Haloperidol
Phenothiazines
188
Essential tremor (benign familial tremor) clinical presentation
Postural or kinetic tremor of both hands and may involve the head or voice
Can begin in early adulthood but often not until later in life
Usually progresses slowly over year to decades
Usually does not results in significant disability, but social embarrassment is common
EtOH often decreases the tremor temporarily
189
Treat essential tremor
Beta blockers
Primidone
Benzodiazepines
Topiramate
Deep brain stimulation
190
Dementia
Decline in memory and at least one other cognitive function (aphasia, apraxia, agnosia, exucitve function)
-decline impairs social or occupational functioning in comparison with previous functioning. These deficits should not occur exclusively during the course of delirium and should not be accounted for by another psychiatric condition such as depression or schizophrenia
191
Incidence and prevalence of dementia
10% over 65
| More than 30% over 85
192
Causes of dementia
```
Degeneration
Vascular
Infectious
Psychiatric (including alcohol)
Toxic/metabolits(B12, thyroid)
Traumatic
Tumors(astrocytoma/glioblastoms, lymphoma, metastatic tumor)
Other(hydrocephalus)
```
193
Evaluation of patient with dementia
History, patient difficulting (safety, function, memory, time course, family history dementia)
Mental status test
Look for CVD risk factors
Full neurologic exam
Lab-CBC, chemistrypanel, Syed rate, thyroid function studies, RPR, CT or MRI of the head, EEG, LP, HIV, CXR, drug screen, SPECT, PET< heavy metal
194
Diagnosis of AD
Dementia (mini mental state exam)
Deficits in 2 or more ares of cognition
Progressive worsening of memory and other cognitive function
No disturbance of consiousness
Onset between te ages of 40 and 90 yr, most often after65
Absence of a systemic disorder or other brain diseases that in and of themselves could account for the progressive deficits in memory and cognition
195
Supporting finding in the diagnosis of probably AD
Progressive deterioration of specific cognitive function such as aphasia, apraxia, or agnosia
Impaired activities of daily living and altered patterns of behavior
Family history of similar disorders, particularly if confirmed neuropathologically
Normal LP
EEG: normal or mild generalized slowing
Progressive atrophy documented by MRI or CT brain
196
Treat AD
```
Slow progression
Acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine)
```
NMDA receptor antagonist (Memantine)B complex, lipid lowering agent, asprin
197
Mild cognitive impairment
Memory complaint, often noted by the patient
Tested abnormal memory for age, and yet does not meet the criteria for dementia(normal cognitive function and daily living)
Probably a precursor to AD
Patients with MCI are 5x more likely to develop clinically probably AD than age matched control s
Treatment with AchEI medications may slow progression to AD
198
Criteria for vascular dementia
1. Cerebrovascular disease defined by the presence of focal signs neurologic examination, such as hemiparesis, lower facial weakness, babinski sign, sensory deficit, hemianopia, consistent with stroke
2. Evidence of relevant cerebrovascular disease at brain imaging including multiple large vessel infarcts or a single strategically situated infarct(angular gyrus, thalamus, basal forebrain, or posterior or anterior cerebral artery territories), as well as multiple basal gangliaand white matter lesions and white matter lacunas or extensive periventricular white matter lesions or combination threof
3. A relation between cognitive problems and vascular events manifested or inferred by the presence of one or more of the following
- onset of dementia within 3 months after a recognized stroke
- abrupt deterioration in cognitive function OR
- fluctuating, stepwise progression of cognitive deficits
199
Diffuse Lewy body disease
Dementia, parkinsonian, prominent psychotic symptoms, EXTREME SENSITIVITY TO ANTIPSYCHOTIC AGENTS
200
Diffuse Lewy body disease
- often progresses more rapidly than AD
- symptoms generally vary a great deal more from one day to the next than do symptoms in AD
- up to 81% of patients with diffuse ley body have unexplained periods of markedly increased confusion that last days to weeks and closely mimic delirium
- mild to moderate parkinsonian features are often present early int he disease. Bradykinesia, rigidity and falls are often prominent. Tremor is usually absent. Response to L dopa is poor
- dysautonomia is common
- psychotic symptoms are mush more common and occur earlier in diffuse Lewy body disease that AD
- visual hallucinations is the most common psychotic symptom-generally animals or people, often children
- these hallucinations are often not particularly bothersome
201
Beware. Most patients with diffuse Lewy body disease experience severe, potentially life-threatening adverse reactions if treated with ___ ___
Antipsychotic agents
If an antipsychotic is truly needed, use one of the newer agents (quetiapine or olanzapine)
202
Parkinson
Midbrain Lewy bodies
Executive dementia sometimes occurs late in illness
Resting tremor usually resent
Autonomic dysfunction sometimes seen
Hallucinations only in response to anti parkinsonian drugs
203
Diffuse Lewy body disease
Cortical Lewy bodies
Cortical dementia always occurs early in illness
Resting tremor usually absent
Autonomic dysfunction prominent
Hallucinations common in absence of anti parkinsonian drugs
204
Frontotemporal degeneration
Progressive deterioration of social skills and changes in personality, along with impairment of intellect, memory and language
Varies greatly int he way it affects individuals, but often see common core symptoms(loss of memory, lack of spontaneity, difficulty in thinking or concentrating, disturbances of speech)
Other symptoms include:gradular emotional dullness, loss of moral judgement, and progressive dementia
Usually affects individuals between ages 40 and 60
Patients typically have atrophy of the frontal and temporal lobes of the brain
No cure. Length progression 2-10 years
205
Triad of hydrocephalus
Dementia
Gait
Urinary incontinence
206
Hydrocephalus is potentially reversible with ____ ___
Ventriculoperitoneal shunting
207
What symptom is most likely to be reversed in normal pressure hydrocephalus with ventriculoperitoneal shunting
Gait
208
CADASIL
Cerebral autosomal dominant ubcortical infarcts and leukoencephalopathy
209
Onset CADASIL
40-50
210
Inheritance CADASIL
NOTCH3 gene on chromosome 18 causing progressice degeneration of smooth muscle cells in BV
211
Manifestation of CADASIL
Migraine HA and TIA or strokes. MRI shows abnormalities of multiple areas of ischemia years prior to the onset of symptoms
212
Progression of CADASIL
Subcortical dementia
213
Treating CADASEIL
Genetic test and sometimes skin biopsy to look for typical arteriopathy
214
Treat CADASIL
Antiplatelet agents, and efforts to minimize risk factors for vascular disease are helpful
No specific treatment
215
Stroke
5th leading cause of death in US, leading to long term disability, 133000 die annually, survivors have residual impairment , pregnancy and post partum
216
Subtypes of. Stroke
Hemorrhagic and ischemis
217
Hemorrhagic stroke 20%
```
Intracerebral hemorrhage (cortical vs subcortical)
Subarachnoid hemorrhage
```
218
Ischemic stroke 80%
```
Large artery atherosclerosis with thromboembolism
Small vessel (lacunar ) disease
Cardioembolism
Nonatherosclerotic vasculopathies
Hypercoagulable states
```
219
Risk factors for stroke
```
Age
Previous TIA or stroke
Atherosclerosis
CVD
Drug abuse
Oral contraceptive
Pregnancy post partum
Fibromuscular dysplasia
Hypercoagulable states
Inflammatory disorders
```
220
Symptom of stroke in left hemisphere
Aphasia, right sizes sensory symptoms, right sided motor symptoms, right visual field cut
221
Symptoms of right hemisphere stroke
Left hemineglect, left sided sensory symptoms, left sided motor symptoms, left visual field cut,
222
Symptoms of cerebellar stroke
Ipsilateral ataxia, vertigo, nystagmus
223
Symptoms of brainstem stroke
Cranial nerve findings with contralateral hemisensory or hemimotos symptoms, vertigo
224
Generate management of stroke
Primary prevention, management of the acute stroke
Prevention or control of medical complications (complications account for 50% of death)
Rehab
Prevention of recurrent stroke
225
Emergent diagnosis and treatment of stroke
```
ABS, BP, pulse, cardiac monitor, EKG, O2 saturation
IV access
Neurological examination
Labs
NIH stroke scale
```
226
Acute HTN is common in acute ischemic stroke and in msot cases should __ be treated
Not
227
The area of infarction may have lost autoregularoy function, so that normal BP may be relatively ___ in the brain
Hypotension
228
All stroke patients need IV access
Should not include glucose as hyperglycemia is associated with worse neurologic outcomes
If tPA is a consideration two IV access sites will be needed to eliminate venipuncture after infusion
229
Labs for stroke
CBC, PT, PTT, full chemistry panel and fingerstick glucose, UA, CXR
230
The NIH scale is important if tPA or intra-arterial intervention is a consideration. Describe scores
Score ranges from )(normal) to 43 (coma) and can be used to predict hemorrhagic conversion as well as indication for potential intra-arterial intervention
Score<10=2-3% risk of hemorrhage
Score>20-17% risk of hemorrhage
231
Summary of Eval and tax of acute stroke
```
Maintain ABS
Elevate HOB 30 degrees
O3 3 liters per NC
Vitals, establish IV with NX
CBC, PT, PTT, Chem
EKG
Obtain patient weight
Try to identify cause and treat fever if present
Get history CT
```
232
What history is important for stroke
```
Last time without symptoms
Trauma cause onset
Warfarin/heparin or NOAC?
Symptoms of MI
Symptoms of intracranial hemorrhage
```
233
CT findings stroke
Cerebral infarction (if patient meets all tPA criteria, consider administering tPA if absolutely sure of time deficits began
Normal -consider another cause:seizure, migraine, hypoglycemia
-if history most consistent with ischemia, consider tPA or other therapies (ASA, aggrenox, ticlid, plavix)
234
IV tPA with stroke eligibility criteria
Over 18
Diagnosis of ischemic stroke with clinically apparent neurological deficits
No stroke or head trauma in preceding 3 months
No major surgery in preceding 14 days
No h/o intracranial hemorrhage
No rapidly resolving symptoms or only minor symptoms of stroke
No symptoms suggestive of SAH
No GI or GU hemorrhage preceding 21 days
No symptoms suggestive SAH
No arterial puncture at non compressible site in preceding 7 days
No seizure at onset of symptoms
PT<15 sec or INR<1.7 without warfarin
PTT within normal range if heparin awas given in preceding 48 hours
Platele ycount >1000000
Blood glucose>50 mg/dl
SBP<185 and CBP<110 mmhg and no need for aggressive measures to lower BP
235
How treat acute ischemic stroke with IV tPA
- infuse tPA at a dose of .9mg/kg (max 90mg) over a 60 min. Period with the first 10% of the dose given as a bonus over a 1 min period
- perform neuro assessments and check BP q 15 min. During infusion every 30 min. For 6. Hours after and then every 60 min for the next 12 hours
- if severe HA, acute HTN, or NV occur, stop infusion and obtain an emergent CT head
- If SBP>180 or DBP>105 mmHg, check BP more frequently and give anti-HTN drugs as needed to maintain BP at below those levels
236
Anticoagulation and stroke
Acute anticoagulation with heparin was sometimes used in past to
-prevent of limit progression in patients with acute atherothrombotic infarction, or prevent recurrent embolism in patients with cardio embolic stroke
Early studies suggest 50% reduction int he chance of neurologic worsening, particularly for subcategories of TIA and stroke in progression
-but bad....little role of anticoagulation ins trope patients
237
Other agents to treat stroke
```
Asprin
Aggrenox
Ticlopidine
Clopidogrel
Dipryidamole
Warfarin
Low molecule weight heparin
Dagibatran etexilate
Riveroxaban
Apixaban
```
238
What are the clinical situations in which warfarin (NOACs are newer) indicated for
```
Atrial fibrillation
Prosthetic valve
MI
Atrial septal defect
Hypocoagulable state
Large vessel disease
Aortic arch disease
```
239
Combination therapy for stroke
ASA and plavix-espicially in the first few weeks after stroke (avoid long term due to increased risk of GI bleeding)
240
In addition to emergent CT scanning of hte brain, what other studies may be done for stroke
CT perfusion studies, MRI, MRA, diffusion weighted and perfusion weighted MRI, transcranial soppler ultrasonography, CT angiography, xenon enhanced CT, single photon emission CT and cerebral angiography
The above test would be selected to establish the anatomical regions and structures involved and the cause of the infarct , thereby choosing appropriate intervention
241
Carotid angioplasty with stent placement
Early data says lower risk of complications than CEA
Consider when patient at high risk for surgery-CAG or valvular heart disease carotid disease or bilateral severe carotid disease
242
Endovasculr therapy(intra-arterial thrombolysis with clot retrieval
MOST PROMISING
SIGNIFICANT IMPROVEMENT IN PATIENT OUTCOME COMPARED TO STANDARD THERAPY
MULTIPLE STUDIES WHOWING IMPROVEMENT IN PATIENTS TREATED WITH ENDOVASCULAR/INTRA-ATERAIAL INTERVENTION IN ADDITION TO TPA WHEN COMPARED TO TPA USE ALONE
243
ACUTE ISCHEMIC STROKE IS AN _____
Emergency
244
How can we get patients to ER sooner
Learn symptoms and signs for early ischemis
245
First thing ask when see patient
Can it be localized?
246
Speech disturbance
Left cortical hemisphere localized
247
Patient sleepy and weak all over
Not localized
248
Number one thing after history and exam
Can i localize it
249
Second thing
Broad categories of what might be causing presentation
250
80 yr old patient with a fib dimished heart function cant speak or move right side
Stroke
251
Broad categories
Congenital/genetic, vascular, tumor/paraneoplastic, infection, inflammation/autoimmune.toxic/metabolic/degenerative/episodic/psychiatric
252
3rd thing
Design testing and treatment plan keeping in mind differential diagnosis
253
Can things be in both categories
Yea vascular genetic
254
Episodic disorder
Migraines?
255
Todd’s paralysis
Can’t speak weakness on right side
256
Primary migraines
Cluster
| Tension
257
Classic
Aura
258
Common
Without aura
259
Aura
Anything neurological but most commonly visual usually 15-30 minutes
260
Migraine F or M
F
261
Age onset migraine
20-30
262
Severity headache
Moderate to severe
263
Quality headache migraine
Throbbing, sharp, severe pressure,
264
Associated symptoms migraine
Nausea, photophobia, sensitivity to light, phonophobia/sonophobia,
265
How long are migraines
Hours to days
266
Trigger migraine
Unknown, stress/letdown , food (MSG), sharp cheese, red wine , chocolate, any food, bright lights, sleep deprivation, change in sleep cycle, hormones (estrogen, BCP, hysterectomy, onset menses, ovulation, exogenous hormone (not progesterone), weather change(storms), smells,
267
chronic migraine
Chronic migraine 15 or more head ache days over 4 hours for at least 3 months -don’t have to be severe, often dull achey
268
Drug of choice for chronic migraine
Only FDA approved is Botox injections done every 90 days
269
Cluster headache
Vascular, men, unilateral, periorbiatal, sharp boring, penetrating, once pick, severe, excruciating, pacing and rocking, can’t sit still, last 45 minutes (5 hours is not cluster), can occur more than once in day, often seasonal FALL
270
Prevent cluster headache long term treatment -when get 2 or three times a year or its not predictable then they get
Verapamil is more common oral (ca channel blocker)**, fewer side effect
Valproic acid-but not young women, get fat on it too
Lithium
271
Prednisone/steroids cluster head ache REACTIVE get it in December for example-start when get cluster headache
Treat
| Cluster head ache give if get once one for a few weeks
272
Who do we not give valproic
Young women unless absolutely no other option
273
Other cluster symptoms
Burning nostril and inner canthus of eye on side, flushing of face on that side
Sleep apnea
274
Secondary headache
```
Worrisome or sign of organic disease
Worst head ache of life
Over 50
Abrupt
Abnormal exam
Loss of sensation
Weakness on one side
Babinksi
Visual field cut
Toe up
Fever
DO WORKUP IF HAVE THIS
```
275
Presentation for ruptured cerebral hemorrhage
Thunderclap headache, severe abrupt onset headache , grab head scream OMG my head and fell down,
276
PCOM posterior cerebral artery symptoms -uncal herniation
CN3 palsy eye down and out
Pupil dilated no parasympathetic (parasympathetic fibers run along outside of third nerve so aneurysm push on it , hit parasympathetic fist)
1st see blown dilated pupil as prescribed harder then get down and out hit axons of third nerve /and stuperous
3 hours later-patient not responsive cant arouse and funny movements DECEREBRATE POSTURING ON CONTRALATERAL SIDE
Bad sign get on phone with neurosurgeon
277
What test when see the pupil in and out and stupor
Put in CT now! Look for subarachnoid hemorrhage
Bright white see it surrounding meninges
278
What do when see subarachnoid hemorrhage on CT
Sedate, ventilation, call neurosurgeon, DO NOT NEED LP not safe
279
What if CT is negative for subarachnoid hemorrhage
LP could be 5-10% of subarachnoid hemorrhage on CT and need LP to look for it and rule out other stuff
280
Trigeminal neuralgia
Pain sharp electrical pain in little paraoxysms last seconds maybe a minute or two
Off and on all day long
Little in and out
281
What triggers trigeminal neuralgia
Chewing talking hot liquids cold liquids frozen food super hot foods brush teeth
282
Drug for trigeminal neuralgia
Carbamazepine
| Oxcarbazepine-better
283
Wilson’s disease
Liver and brain
Copper
Young ppl
284
Don’t catch Wilson
Fatal
285
Wilson treat
Reverse or cure
286
Bradykinetic or hyperkinetic wilson
Both
287
Balism
Large flinging
288
Brief dance like fidget/tic
Chorea
289
Sustained position extension arm extension finger(can get lot of places
Dystonia
290
Myoclonus brief jerking movements
Ok
291
Friedreich ataxia
1. Ataxia (falls, balance disturbance, dimished strength, areflexia)
2. Young ppl
3. Die from cardiomyopathy
292
Akinetic rigid syndromes
Parkinson
293
Most common parkin
Idiopathic PD
294
Features parkinson
Tremor resting or pill rolling UNILATERAL(idiopathic), rigidity, Brady, soft voice, stare, dimished eye blink, myerson sign(tap on forehead),
295
Drug induced parkinson
Bilateral
296
MSA
Autonomic dysfunction pronounced with stiffness and slow
297
CBD
Cortical
| Hemiparesis, apraxia, stiff slow
298
PSP
Eyes vertical gaze
Volitional
If more head eyes do what supposed
If ask them to move up and down they cant
299
Lewy body disease
Slow stiff
Dementia
Hallucinations (visual-little mice, imposter syndrome)-can get in parkinson but only in drug induced parkinson
Early psychotic visual hallucinations
Akinetic and rigid family say they fall all the time often backwards
-delirium are way off encephalopathic
80% crazy then back to self
-don’t treat automatically bc very sensitive to antipsychotic meds and can be life threatening
300
AD
Memory loss
Progresses
At least 2 domains (memory loss and speech disturbance) can become psychotic as well(late-kids try to steal money or spouse having affair, or someone stole stuff when misplaced often directed at people they’re closest to) in Lewy body psychotic is early
301
MS
Central nervous system (spine brain) not peripheral
302
Most common MS
Relapsing remitting MS -exacerbations and remissions , have spell and get better then have another attack
Test cant diagnose 1
Look for MRI, LP, oligoclonal bands igG synthesis rate index igG immunoglobulin and sample of blood ratio igG and CSF to blood in case of MS see abnormalities have more igG in spinal fluid than blood .
Index up synthesis up
303
Recognize disease modifying MS meds on routine maintence basis
Leterium acetate, monoclonal antibodies (MABS-MAB at end)
Interferons, dimethylfumurate, fingolamide
These are not for symptomatic treatment they are disease modifying to change course of disease
304
Drugs for acute attack of MS/shorten course of exacerbation but don’t change overall course of disease
Corticosteroids
IV prenisolone
ACTH acthar gel
STEROIDS
305
Spasticity med
Baclophan
| Trendazoline
306
Neuropathic pain
Pregabalin
307
Stimulants
Methylfenodarte for severe fatigue
308
Mimickers of MS
Clinically isolated syndrome
- monofolcal (1 lesion correlated with 1 symptom
- multifocal, acute disseminated myeloencephalitis can be confused and become MS(multiple lesions at 1 time, wait to see if have MS or one and done —-MS is multiple over space and time)
309
Epilepsy
Partial or focal can secondarily generalize-begin on one side
(Kindling could spread to major motor generalized seizure)
Primary general-
Idiopathic genetic, both sides
310
Generalhow many need to have epilepsy
2 or more unprovoked—alcohol withdrawal doesn’t count, what if one happened with tramadol or something NO not unprovoked
In certain cases can make diagnoses with one seizure and abnormal EG
311
Most important to epilepsy diagnosis
History form witness———what did they look like
312
EEG normal and think have epilepsy
Can miss it may have epilepsy
313
What if see episode on EEG but don’t think epilepsy
Don’t have
314
99% seizure on EEG
Absence seizure wha3 hz spike per second
Starts on both sides of brain initially
Primary generalized or idiopathic
315
Absence
Ethosuximite
316
If major motor seizure and absence
Ethosuximite and broad spectrum whether partial or generalized
1. Valproic acid (not young woman)
2. lamotrogine-works and lowest side effects and safe in pregnancy 2/3 patients first drug will work
3. Levotoracitam
4. Zonisamide
317
Zonisamide and topiramate
Kidney stones-so if history move to something else
318
Try to use one drug or more
1
319
New are better and new effective
Start with newer drugs
320
Most common reason for breakthrough seizure in well controlled for years
Noncompliance missed meds
321
Absence
Abrupt stop and abrupt start on ecg
322
What can accompany major motor seizure
Lateral part of tongue bite
Urination , bowel incontance
Post ictal state-lethargic tired confused
323
Transient global amnesia
```
1 and done does not recur
Amnesia only ! Lasts hours 3-6
Patient asks the same questions over and over again scares people
By time consult comes its resolved
Very common
```
324
Stroke
Sudden like lightening
325
2 types stroke
Ischemic-80%
| Hemorrhagic 20%
326
Risk for stroke
Hypertension, tobacco, age, DM, TIA or previous stroke, cardiac arrhythmia, A fib high risk, mural thrombas from old MI, left ventricle from heart attack, idiopathic, cardiomyopathy, not pumping does sound familiar, ejection fraction measure how much blood pumped out 2-% or less bad ventricular function high risk of getting clot on left ventricle that shoot out that’s the 20%
327
Med to prevent stroke
Asprin
| Clavix,
328
Multiple stroke treat A fib, ejection fraction less than 20% (cardiomyopathy) prevention of stroke , prosthetic valve
To prevent still not at treatment
Warfarin or NOAC(newer oral anti coagulation)
329
Acute stroke
Don’t want glucose blood sugar?
Passive hypertension to increase perfusion
(Don’t want to lower it) allow for a while (let it be high for 2 weeks then manage it)
Fever
ABC always check
330
Treat acute stroke
Ok
331
What can cause focal neurologic prob and be confused with stroke ABRUPT
Primary headache disorder migraine with aura (tingling, work finding difficulty)
Metabolic abnormalities
Hyperglycemia
Hepatic
332
Coma
Both cerebral hemispheres effected or brainstem effected
333
Lesion in pons
Coma
334
Lesion in medulla
Coma
335
Small thalamus, hypothalamus, one side
No need both hemispheres
336
What is periventricular white matter abnormalities on both side
No haven’t effected cortex so no coma
337
Coma from herniation hallmark
Anesecoria, pupillary abnormality -don’t see if have hepatic dysfunction or glucose stuff
338
Hepatic encephalopathy examination-can get neurologic
Asterixis
| Extend arms extend wrist see twitchy movements
339
Progression of loss of function in brain of anoxic patients reverse teleological area. Oldest teleological most resistant to anoxia
First lose most well developed(last to develope are first to go)-cortex
2. Lose corneal reflex and pupillary responses level of midbrain
3. Oculocephalic-mid pone (water in ear)
340
Mild anoxia
Memory loss confusion
341
Brain death
Specific definition know it
342
Patient has 103 fever stiff neck encephalopathic or comatose
ABC
O2 state, EKG, glucose, CBC, CMP , quick history
Cat scan negative then do LP
343
If diffuse edema and herniation on cat scan
Do not do LP brain stem herniation into spinal canal
344
AD vs Lewy body
Hallucinations early lewy-usually visual
| Hallucination late in AD-usually paranoia
345
1st AD
Short term memory language word finding can get paranoid or aggressive later on
346
MRI Ad
Generalized atrophy
347
Normal pressure hydrocephalus triad
Gait-falling
Urinary incontinence
Dementia (cognitive impairment )
348
NPH
Progressive onset in less than a year
349
MRI NPH
Enlarged ventricles without obvious obstruction
350
Treat NPH
Shunt neurosurgeon shunt decrease space of ventricles sometimes help sometimes not
Gait improves first
351
Vascular dementia —hemiparesis upgoing to, sensory loss incordination in one hand, visual field cut-something says focal
Step wise progression-fine fine fine then terrible stable stable stable, another abrupt —multiple over time take patient down
Or
Massive single strategically placed stroke-left hemisphere cant communicate and demented unless improve
ONE event
352
Nystagmus of labrinthial
Horizontal nystagmus
Don’t see vertical or pendular nystagmus
353
Ménière’s disease
Hearing los
Low frequency
Tinnitus -crickets high frequency , high pitched funny noise cant go to sleep, dull fullness sensation in ear. Funny fullness sensation
Most of people lose high frequency
354
Teat menieres
Low sodium diet
Diuretics
Low dose Valium will also fix
355
Toxins that can cause vestibular dysfunction
Alcohol and
Chronic-cerebellar dysfunction can cause
Antibiotics-aminoglycocides gentomycin
356
Rhomberg test
Feet together arms to side close eyes
If able to stand with eyes open ok then close and cant keep balance
Have proprioceptive abnormality rhomberg positive
Testing proprioceptive pathways
357
Benign paroxysmal vertigo initially presentation BPPB
Patient awakens and feel fine don’t
Severe vertigo vomiting nausea, cant keep balance ,
358
What do to test BPPV POSITIONAL one position fine other and not fine
Dicks hall pike maneuver turn one way ok turn other way and get symptoms tells us labyrinth and BPPV
Vestibular neuritis is also labyrinth and no different in turning other way
359
Orthostatic hypotension
Laying to standing systolic change 20 diastolic Change of 10
Describe light headed dizzy faint when upright head
Dizzy upon standing relieve symptoms when lay down
Also worse in morning -been flat long time
360
MS drugs disease modifying change overal outcome
Interferons, monoclonal antibodies, literium acetate, dimethylfumerate
361
Steroids
Not disease modifying
362
Symptom treatment spasticity
Baclofen ????
363
Gabapentin pregambalin
Neuropathic pain
364
3d diffusion tensor imaging
Look for axonal injury in periventricularwhite matter
365
Student athlete concussion and headache nausea
Do not let them do sport
366
Student athlete no symptoms
May let them do light aerobic exercise
367
Mild symptoms
Sit out
368
When see again
A few days later
369
Symptoms after aerobic exercise
Sit
370
Treatment for consussion
Rest
371
Dopamine vs serotonin effective
Dopamine-cognition OK, compulsive(reward system), irritable,
Serotonin SSRI-inhibit reuptake, treat mood disorders-have mood disorders, depression, irritability, anxiety, decreased COGNITION, sleep disturbance,
