2.
Risk Factors - Stroke
Age >50
Family history of CAD, CVD, or PVD before age 60
Clinical manifestations of CAD or PVD
Hypertension
Diabetes mellitus
Elevated cholesterol
Smoking
Hyperhomocysteinemia
Carotid bruit ( presene only if luminal stenosis >50%)
History of TIA
History of paroxysmal or persistent atrial fibrillation
3.
Primary Prevention Of Stroke
Control hypertension Use ACE
inhibitor in high-risk patients if they
are hypertensive or diabetic, or if they
have already had a vascular ischemic
event.
Smoking cessation.
Achieve glycemic control in diabeteics
Start warfarin in most patients with
nonvalvular atrial fibrillation in whom
sinus rhythm cannot be restored,
including (CHADS2)
High-risk patients with previous embolization
(TIA/CVA), age > 75, HTN, DM Type II and
those with congestive heart failure or
decreased left ventricular function
Elderly patients to maintain an INR between
1.8 and 2.5
4. Primary Prevention Of Stroke
Do not use warfarin in patients who cannot have
adequate monitoring of INR, cannot receive medications
in a predictable fashion, or have increased risk for
bleeding (i.e., those with a high risk of traumatic fall
(elderly), those with high-risk occupations, or those who
have a bleeding disorder).
Start antiplatelet therapy in Afib for prevention for
storke- ASA 50 to 325 mg po qd, Clopidogrel, 75 mg po
qd, or Aggrenox
- in low-risk patients with nonvalvular atrial
fibrillation (lone afib)
- in higher-risk patients who decline
anticoagulation, would not comply with INR monitoring, or
are at very high risk for bleeding.
Discontinue combination estrogen and progestin
treatment in healthy postmenopausal women.
Consider starting low-dose every-other-day aspirin in
otherwise asymptomatic women over the age of 45.
5. Primary Prevention - Stroke
Carotid endarterectomy should be
considered in asymptomatic
patients with >60% stenosis who
have no other contraindications for
surgery (especially severe
cardiopulmonary disease), are
under age 75, and are expected to
live >5 years .
6. Stroke - Management
Immediate Neurologic Assessment (<25 minutes)
Alert Stroke Team of possible Thrombolytic. Determine onset of CVA
symptoms Consider Thrombolytics within 3 hours of onset
Physical Examination Neurologic Examination Assess Level of
Consciousness (Glascow Coma Scale) & Assess Stroke Severity
Step 2: Rule-out Hemorrhagic CVA
Imaging
If Head CT suggests intracranial bleeding Neurosurgery consultation
Reverse anticoagulants or Bleeding Disorder and Manage Hypertension
appropriately
Head CT negative despite high suspicion for SAH
Obtain urgent noncontrast Head CT (<25 minutes) Head CT read by
radiologist (<45 minutes)
Lateral Neck XRay Indications Altered Level of Consciousness , Trauma
Obtain Lumbar Puncture to assess subarachnoid blood remember,
Lumbar Puncture contraindicates Thrombolytics if you are
suspecting an ischemic cva also.
Head CT negative suggesting Ischemic CVA
Give Thrombolytic Therapy if meets the criteria/ If not, just ASA or
Aggrenox.
8. Stroke - Thrombolytics
Inclusion Criteria
Age over 18 years
Clinical Diagnosis of acute Ischemic Stroke
CT Head compatible with Ischemic CVA diagnosis
Known time of onset under 3 hours before Thrombolytics
Do not use intravenous tPA beyond 3 hours of symptoms
Exclusion Criteria
Improving or mild neurologic deficit
Seizure at onset
Head Injury or CVA within 90 days
History of Intracranial Hemorrhage
Suspected Subarachnoid Hemorrhage (SAH) Hemorrhage on CT Head or History
suggests SAH even despite negative Head CT (worst headache/ photophobia)
Hypertension refractory to antihypertensives Systolic Blood Pressure over 185 and
Diastolic Blood Pressure over 110 ( if elevated, control and then give tpa)
Major surgery in last 14 days
Gastrointestinal hemorrhage in last 21 days
Genitourinary hemorrhage in last 21 days
Puncture of inaccessible artery within 7 days
Coagulation or Platelet abnormalities
9. Thrombolysis Protocol
t-PA (Alteplase) – given 1 time over 1 hr IV
Manage Blood Pressure aggressively postThrombolytic Keep SBP < 185 & DBP < 105
Observe in ICU for first 24 hours
No other antithrombotic agents/ aspirin/
anticoagulants should be given for next 24 hours
(many ppl have this doubt with unstable PE
management also – no heparin for 24 hrs!)
CT Head at 72 hours
10. Stroke – Other Rx
Start Aspirin 325 mg daily after an ischemic stroke/ TIA.
Heparin/ LMWH has no role in treatment and has increased bleeding risk
( should be used only for DVT prophylaxis not for treatment of CVA)
Later Start aggrenox for secondary prevention of stroke
Warfarin has no additional advantage over Aspirin – do not use unless
indicated.
Remember complications in acute stroke like SIADH, Pneumonia, UTI and
treat adequately
DVT prophylaxis – all cases ( in hemorrhagic stroke ?? may start within 48
hours)
BP Control
Don’t lower Blood Pressure too low in acute CVA Lower Blood Pressure
leads to lower perfusion in ischemic CVA
Absolute indications for BP intervention in acute Ischemic CVA
Blood Pressure >220/120 or MAP>140
Target organ dysfunction (Hypertensive Emergencies) Acute Myocardial
Infarction, Hypertensive encephalopathy, Renal Failure, Aortic Dissection
or Retinal hemorrhage / papilledema.
In haemorrhagic stroke, drop SBP by 25-30% ( preferably keep it around 160
range) put an A-line , use labetalol/ nitroprusside drips if needed
11. Stroke Prevention – Antiplatelet
therapy comparision
Treat all patients with ischemic stroke or TIA
with aspirin, 50 to 325 mg/d.
Recognize that aspirin, 25 mg, plus extendedrelease dipyridamole, 200 mg bid, both given
bid, is superior to aspirin alone and should be
considered in all patients with TIA or stroke,
although it is more expensive.
Consider clopidogrel alone, 75 mg/d, in patients
who cannot tolerate aspirin, as it has similar
efficacy to aspirin alone.
12. Stroke – Other Rx/ Secondary Prevention
Evaluate for carotid stenosis ( carotid u/s)
Evaluate for atrial fibrillation (ekg)
Evaluate for structural heart disease etc
( 2D echo)
Rx if Hyperlipidemia is present ( Ischemic
thrombotic CVA is CAD equivalent).
Tobacco cessation
13. Carotid Stenosis
Evaluation
Carotid Artery Duplex Ultrasonography
Standard diagnostic tool for carotid stenosis
Less expensive than MRA
Accuracy for diagnosing severe carotid stenosis
Test Sensitivity: 86% , Test Specificity: 87%
Carotid Magnetic Resonance Angiography
(MRA)
Better than ultrasound at defining carotid anatomy
Accuracy for diagnosing severe carotid stenosis
Test Sensitivity: 95% , Test Specificity: 90%
14. Symptomatic Carotid Stenosis -Mx
Remember that Endarterectomy carries risk of
significant morbidity
Cognitive changes can occur and there can be a 7% risk of
CVA within 30 days of procedure
Symptomatic patient with carotid stenosis >70%
These patients will significantly benefit from carotid
endarterectomy, even if they are over age 75 years
Symptomatic patient with carotid stenosis 50 to 69%
Benefit from carotid endarterectomy present, even if they are
age > 75yrs. However, here consider it if pt is likely to live >
5yrs
Symptomatic patient with carotid stenosis <50%
No benefit from carotid endarterectomy – do not recommend!
Use all other secondary prevention measures
15. Asymptomatic Carotid Stenosis > 60% Management
Medical therapy: 5 year risk of CVA 12%
Hypertension control
Hyperlipidemia control with Statins
Clopidogrel (Plavix)
Surgical Procedures: 5 year risk of CVA 6%
Carotid endarterectomy or
Angioplasty & carotid stenting ( stenting
can be considered in In symptomatic, highrisk candidates for carotid endarterectomy
& In patients with surgically
unapproachable stenosis)
17. Intracerebral Hemorrhage (ICH)
In any patient with stroke symptoms, obtain NON-CONTRAST CT head
first to r/o hemorrhagic stroke
Most common cause is HTN. Other causes are amyloid angiopathy,
vascular malformations, coagulopathy and cocaine abuse
Clues for Amyloid angiopathy – primarily a lobar hemorrhage and seen
mostly in elderly.
Obtain cerebral angogram to rule out vascular malformations in :
Patients with ICH who are age under 45
Patients who developed ICH after cocaine use
Rx control BP to maintain SBP between 140 and 160 mm hg ( use IV
labetalol or nitroprusside or nicardipine)
Mannitol and Hyperventilation to reduce intra cranial pressure
In intracerebellar hemorrhages, realize that its very close to brain stem –
so a mass effect can lead to Brain stem herniation. So, in intracerebellar
hemorrhage, if extensive, will need URGENT SURGICAL
DECOMPRESSION – contact neurosurgeon STAT!
18.
Subarachnoid Hemorrhage
Common causes : Berry aneurysms, AV malformations, Neoplasms
C/F: Severe headache, photophobia, loss of consciousness, papilledema
Prevention :
Obtain MRA to screen for Berry aneurysms in patients with ADPKD
only if family member is diagnosed with an Intra Cranial Aneurysm or
SAH, if the patient refers to symptoms related to an ICA or a patient
has a high risk job
In patients with incidental aneurysms, if size > 10 mm surgery. If
size < 10mm, follow up MRI in 1 to 2yrs.
Diagnosis : Non contrast CT first. If CT –VE, LP if suspicion is high look
for xanthochromia ( 10% SAH are missed by CT Scans)
RX
If there is a ruptured aneurysm, rx with surgical clipping in 48 hours
Nimodipine to prevent post subarachnoid hemorrhage vasospasm and
consequent, iscemic stroke ( Vasospasm after SAH is the most
dreaded complication of SAH leads to stroke)
Triple “H” therapy ( Induced Hypertension, hemodilution and
hypervolemia) is also widely used in preventing and treating cerebral
vasospasm after aneurysmal SAH.
20. Meningitis
Symptoms : Fever, Photophobia,
Headache, Neck stiffness, vomiting,
seizures
Use physical exam findings to confirm a
diagnosis of meningitis.
Look for:
Fever
Nuchal rigidity
Brudzinski's sign
Kernig's sign
Signs of encephalitis, such as weakness and change
in mental status
21. Meningitis
Do lumbar puncture to obtain CSF for:
Protein, glucose, and cell count determinations
Gram stain and bacterial culture
PCR testing for enterovirus and HSV if bacterial Gram stain and culture
results are negative and cell counts suggest viral meningitis
Obtain CT scan before lumbar puncture in patients with: ( HIPFAN)
Immunucompromised state (I)
History of CNS disease (H)
New onset seizures (N)
Papilledema (P)
Altered level of consciousness ( suggests encephalitis)(A)
Focal neurologic signs (F)
Be aware that delay in initiating appropriate antibiotics while awaiting
results of CT scan in patients with bacterial meningitis may result in an
adverse clinical outcome.
23. Meningitis – Empiric Rx
Base empiric antibiotic therapy on:
Patient's age
CSF gram-stain result
Potential bacterial pathogens
Knowledge of local resistance patterns for those
pathogens
Thereafter, base targeted antibiotic therapy on
culture results and susceptibility data.
Administer dexamethasone 15 to 20 minutes
before the first antimicrobial dose in adult
patients with suspected meningitis.
24. Meningitis – Emperical therapy
Predisposing Factor
AGE
<1 month
1 - 23 months
2- 50 years
>50 years
Common Bacterial
Pathogens
Antimicrobial Rx
Streptococcus
agalactiae, Escherichia
coli, Listeria
monocytogenes,
Klebsiella species
Streptococcus
pneumoniae , Neisseria
meningitidis, S.
agalactiae,
Haemophilus
influenzae, E. coli
N . meningitidis, S.
pneumoniae
Ampicillin plus
cefotaxime or ampicillin
plus an aminoglycoside
S. pneumoniae, N.
meningitidis, L.
monocytogenes ,
aerobic gram-negative
bacilli
Vancomycin plus a
third-generation
cephalosporin
Vancomycin plus a
third-generation
cephalosporin
Vancomycin plus
ampicillin plus a thirdgeneration
cephalosporin
25. Meningitis – Emperical therapy
Predisposing Factor
Common Bacterial
Pathogens
Antimicrobial Rx
Basilar skull fracture
S. pneumoniae, H.
influenzae, group A
-hemolytic streptococci
Vancomycin plus a thirdgeneration cephalosporin
Penetrating trauma
Staphylococcus aureus,
coagulase-negative
staphylococci (especially
Staphylococcus
epidermidis), aerobic gramnegative bacilli (including
Pseudomonas aeruginosa )
Aerobic gram-negative
bacilli (including P.
aeruginosa ), S . aureus ,
coagulase-negative
staphylococci (especially S.
epidermidis)
Coagulase-negative
staphylococci (especially S.
epidermidis), S. aureus,
aerobic gram-negative
bacilli (including P.
aeruginosa ),
Vancomycin plus cefepime,
vancomycin plus
ceftazidime, or vancomycin
plus meropenem YOU
ARE Adding an
antipseudomonal antibiotic.
HEAD TRAUMA
Postneurosurgery
CSF shunt
Vancomycin plus cefepime,
vancomycin plus
ceftazidime, or vancomycin
plus meropenem
Vancomycin plus cefepime,c
vancomycin plus
ceftazidime,c or vancomycin
plus meropenem
27. FALLS IN ELDERLY
Epidemiology
Falls occur in >30% of age over 65 years in community
Serious injury occurs in >20% of falls in older adults
Most falls occur in and around the patient's home
Risk Factors for falls
Environmental hazards (most common)
Altered gait or balance
Lower extremity Muscle Weakness
Dizziness or Vertigo
Syncope
Postural Hypotension
Decreased visual acquity
Arthritis
Dementia or Altered Level of Consciousness
Major Depression
Medication use (especially more than 4 medications)
Class IA Antiarrhythmics, Digoxin, Diuretics , Anticonvulsants ,
Psychotropic medications like Benzodiazepines & Antipsychotics
28. Screening and Evaluation for fall risk
Get Up and Go Test
Cardiovascular exam
Postural Hypotension , Arrhythmias , Carotid Bruits
Neurologic Exam
Assess coordination and balance , Lower extremity muscle strength
& Proprioception and vibration sense
Miscellaneous exam
Visual Acuity , Joint exam
Diagnostics in cases of fall history
Complete Blood Count
Thyroid Function TeSts
Chemistry panel including Renal Function tests
Serum Vitamin B12
Electrocardiogram
Echocardiogram
Brain Imaging
29. Get up and Go Test
Technique: Direct patient to do the
following
Rise from sitting position
Walk 10 feet
Turn around
Return to chair and sit down
Interpretation
Patient takes <20 seconds to complete test
Adequate for independent transfers and mobility
Patient requires >30 seconds to complete test
Suggests higher dependence and risk of of falls
30. Fall Risk - Prevention
Use Assistive Devices
Wear flat, rubber soled shoes
Use ambulatory aid as needed (cane or
walker)
Consider Hip protection device
Two convex shields worn inside underwear
pocket
Greatly reduces Hip Fracture Incidences
Wearing pads: 0.39 Hip Fractures per 100 falls
Not wearing pads: 2.43 Hip Fractures per 100 falls
May reduce Incidence of pelvic fracture
31. Fall Risk Prevention
Education
Proper lifting technique No stooping; bend knees
and keep back straight
Optimize Comorbid Conditions
Assess number/type of medications
Check Visual Acuity
Vision <20/60 is a risk for falls
Check for Cataracts
Assess for depth perception
Control systolic Hypertension
Systolic Hypertension affects balance and fall risk
Avoid medications that increase fall risk
Medications causing hypotension or Dizziness
Medications causing Sedation
Benzodiazepines
High risk of falls and Hip Fracture
Highest risk within first 2 weeks of starting
32. Fall Risk Prevention
Modify home environment
Consider occupational therapy evaluation
Hand grips and safety mat in shower
Treads and handrails in stairway
Anchor rugs, non-skid rubber mats
Remove clutter, exposed wire, or cord
Keep halls and stairways well lit
Use nightlights in bathrooms and bedrooms
Participate in regular Exercise (30
minutes, 4-5/week)
Walking Program
Exercise classes twice weekly reduces fall risk
35. Migraines - Features
Presence of nausea or vomiting
Duration of typical untreated headache between 4 and
72 hours
Pulsatile or throbbing character
Unilateral location of head pain
Level of disability associated with typical attacks and
impairment of usual daily activities ( any day during past
3 months)
Photophobia and phonophobia
Presence of at least 4 of the symptoms above has
sensitivity of 29% for detecting migraine and specificity
100%
Presence of at least 3 of the symptoms above has
sensitivity 80 and specificity 94
36. Migraine - Features
Consider using the pre-test probability of migraine and
the number of symptoms in the POUND mnemonic to
calculate the post-test probability of migraine.
In applying the mnemonic, determine whether the
headache is:
P ulsatile in quality
Approximately O ne-day's duration (between 4 and 72
hours)
U nilateral in location
Accompanied by N ausea or vomiting
Of D isabling intensity
37. Post-test Probabilities of Migraine Based on the
Number of Migraine Features on History Compared to
a Reference Standard of Headache Expert Neurologist
Clinical Evaluation
Result
Pretest Probability (%)†
20
50
80
5
15
50
3 migraine symptoms*
75
94
99
4 or 5 migraine symptoms*
90
96
>99
0, 1, or 2 migraine symptoms*
38. Migraine - Diagnosis
No need for neuroimaging for migraine patients
and a normal neurologic examination
Obtain imaging only if atypical headache
features ( worst headache, headache awakening
from sleep, headache
Obtain an ESR in patients over age 50 who have
new-onset headache to exclude the possibility of
temporal arteritis. Remember, however, that
an elevated ESR (>30 mm/h) is not diagnostic of
temporal arteritis and that a temporal artery
biopsy is needed for diagnosis.
39. Migraines - Rx
Identify and avoid dietary “triggers,” including:
Caffeine withdrawal , Nitrates and nitrites in
preserved meats, Phenylethylamines in aged
cheeses, red wines, beer, champagne,
chocolate, and monosodium glutamate in Asian
and other prepared foods , Dairy products ,Fatty
foods
Recommend specific behavioral therapies for
migraine patients, including relaxation training,
biofeedback, or cognitive-behavioral therapy
42. Drug Rx
Use migraine-specific agents (e.g., triptans,
dihydroergotamine, ergotamine)
- in patients with severe migraine
- in those whose headaches have
responded poorly to NSAIDs or combination
analgesics such as aspirin plus acetaminophen
plus caffeine.
Triptans first choice because they are more
effective and cause less nausea.
All of these agents are contraindicated in the
presence of CAD. (Ergots contraindicated,
NSAIDS better avoided)
43. Preventive rx
Indications for daily preventive drug treatment in patients with significant
disability related to frequent or severe migraine attacks (usually at least
2 per month):
Recurrent headaches that interfere with daily routine
Contraindication to acute (abortive) therapy , Failure or overuse of
acute therapy , Adverse effects from acute therapy , A preference for
preventive therapy
Choose among the following effective classes of agents, listed in order
of strength of evidence for efficacy:
Non-selective, β-antagonists
Anticonvulsants : VALPROIC ACID, TOPIRAMATE Be aware that
valproate is the only antiepileptic drug approved by the FDA for
migraine
Antidepressants, calcium antagonists, ARB ( Candesartan)
Consider perimenstrual preventive treatment with a triptan for
menstrually associated migraines. ( also ocpills without off period,
Seasonale etc).
Try a drug therapy for at least 2 months before changing the agent.
Consider tapering or discontinuing preventive treatment after a
sustained reduction in headache frequency that lasts 6 to 12 months.
44. Referral
Refer the following to a migraine specialist:
Intractable migraine (status migrainosus)
Medication-overuse headache or chronic
migraine (sometimes described as
“rebound” headache, transformed
migraine, or chronic daily headache)
Analgesic dependency (especially narcotic
analgesics)
46. Cluster Headaches
Excruciating headache pain
Duration of typical attack - 15 to 180 minutes
Symptom-free intervals vary from 1 to 48 hours
Frequency : up to 8 attacks/day
Headache attacks come in clusters daily or at variable
periods.
Nausea, photophobia and phonophobia
Tends to occur more in nights- The headaches have a predilection for
the first rapid eye movement (REM) sleep phase so the cluster patient will awaken
with a severe headache 60 to 90 minutes after falling asleep
Look for presence of autonomic symptoms : Tearing,
Conjunctival injection, Ptosis , Rhinorrhea , Nasal
congestion , Forehead and facial sweating and Miosis
Note the behavior during attacks (usually agitated, unlike
in migraine where the patient is quiet and withdrawn!)
----------edited ---
47. Cluster Headache - Physical
During an attack, look for autonomic features
that will help you diagnose this headache:
Ipsilateral ptosis
Miosis
Eyelid edema
Lacrimation
Rhinorrhea
Nasal congestion
Forehead and facial sweating
Conjunctival injection
ANY OF ABOVE CLUES AT THE TIME OF
HEADACHE CAN HELP IN DIAGNOSIS
48. Investigations
Cluster headache is a clinical diagnosis.
Obtain neuroimaging with MRI and MRA in
patients with:
Atypical headache features OR Abnormalities
on neurologic examination OR Lack of response
to previous treatments
Order an ESR to look for temporal arteritis in
patients over age 50 with headache and visual
loss.
Obtain a polysomnogram in patients with
headache to identify sleep-disordered breathing
(sleep apnea), especially those with snoring or
daytime sleepiness.
49. Treatment
Identify and recommend that patients avoid trigger
factors of cluster headache such as: Alcohol , Smoking ,
Solvents , Altitudes above 5000 feet , High temperatures
, Altered sleep schedules, e.g., afternoon naps, work
shift changes, traveling across time zones, delay or
advanced sleep phase
Acute Rx : Give 100% oxygen administered by
nonrebreather face mask at 7 to 15 L/min for 15 to 30
minutes and repeat as needed.
To treat acute attacks, consider using separately and
then combine as necessary:
Subcutaneous or intranasal sumatriptan, or nasal
zolmitriptan
Intramuscular, subcutaneous, or intravenous DHE
Oral or rectal ergotamine
Other options : oral corticosteroids, Ipsilateral occipital
nerve block
51. Clinical features
Pain lasts from few seconds to minutes.
“Electric” like in character. Can be spontaneous
or triggered by light touch, talking or eating.
Distributed trigeminally (usually second or third
divisions), either alone or in combination
First division pain around the eye or forehead
occurs in 10%-20% of patients, often with pain in
other parts of the face, usually mid-cheek and
upper lip or teeth
Usually unilateral
Pain is relieved by carbamazepine or
oxcarbazepine but not narcotics or milder
analgesics Consider using carbamazepine
administration as a diagnostic maneuver
52. Clinical Features
Refractory period of pain after stimulation
of the trigger area (cannot elicit pain again
by touching or pushing immediately after a
painful attack) Highly predictive of
trigeminal neuralgia.
Neurological exam is usually normal
Note that abnormal neurological findings
are indicative of diseases other than
trigeminal neuralgia.
53. Treatment
Avoid PAIN triggers Stay away from the
direct blast of an air conditioner , Cover
the face before going out into a cold wind,
using covers that do not touch the face or
that are not tight fitting , Avoid foods that
trigger the pain for an individual patient
(e.g., hot or cold drinks, foods that require
much chewing)
54. Treatment
Mild, infrequent pain no treatment
Drug of choice for Trigeminal neuralgia
Oxcarbazepine or Carbamazepine
If pain persists, add another drug, such as
gabapentin, baclofen, lamotrigine, or pregabalin
If pain continues despite drug therapy needs
neurosurgical intervention gamma knife
radiosurgery or percutaneous balloon
microcompression of trigeminal division that is
causing symptoms.
56. Tension Headaches
Most common form of headache
Last from 30 minutes to 7 days
Typically have bilateral location
Have a nonpulsating pressing or tightening quality
described by patients as a “band-like” constriction
around their head,
Are mild to moderate in intensity
Do not prohibit activity. ( Unlike migraines)
There is no aggravation of headache by using stairs or
by doing any similar routine activity; not associated with
nausea or vomiting (although anorexia may occur);
neither associated with both photophobia and
phonophobia (but may exhibit one or the other)
57. Treatment
Try Acetaminophen first
NSAIDS if no response to tylenol. OTC NSAIDS and then
prescription NSAIDS
Combination Medications: Aspirin or acetaminophen (or both of
these analgesics) are often combined with caffeine or a sedative
drug in a single medication. For example, Excedrin combines
aspirin, acetaminophen and caffeine Combination drugs such as
this may be more effective than are pure analgesics for pain relief.
Many combination drugs are available over-the-counter, analgesicsedative combinations can be obtained only by prescription because
they may be addictive and can lead to chronic daily headache.
Advise pts not to use these drugs more than two days a week, as
they can lead to chronic daily headache
Opiates, or narcotics, are rarely used because of their side effects
and potential for dependency. These include codeine combined with
acetaminophen
59. CDH
Chronic daily headache" (CDH) includes a
variety of headache types, of which
chronic migraine is the most common.
Medication overuse, or drug rebound
headache, is the most treatable cause of
refractory daily headache.
A pathologic underlying cause should be
considered in patients with recent-onset
daily headache, a change from a previous
headache pattern, or associated
neurologic or systemic symptoms.
62.
CDH
Most patients with CDH have chronic
(transformed) migraine.
There is a hx of episodic migraine that has
evolved (transformed) over time into a pattern of
almost daily headaches.
These daily headaches may be mild, but
migraine flares may continue to be
superimposed on the daily headache symptoms.
The most common causes of migraine
transformation a)frequent headaches at
baseline and b) obesity.
Other modifiable risk factors for transformation
include medication overuse, snoring, and
stressful life events.
63.
Drug rebound & Medication
overuseto improve despite use of
Patients who do not stop analgesic overuse fail
preventive therapy patients who stop taking analgesics on a daily basis have a
marked reduction in frequency of headache
Drug rebound headache is a common treatable cause of transformed migraine.
Patients who have drug rebound headache are refractory to usual acute and
prophylactic interventions CLUE : The patient who repeatedly presents to the
emergency department requesting narcotics for headache relief most commonly
has drug rebound headache.
The sustained use of these medications more than three days per week is
sufficient to develop drug rebound headache.
All headache medications, including triptans,have the potential to cause drug
rebound headache.
Most common agents that cause drug rebound headache are narcotics, butalbital
products, and combination products containing caffeine.
Be alert to recognize signs of secondary headache in patients who are selfmedicating frequently Only after a careful evaluation for secondary headache
should drug rebound headache be suspected in patients with medication overuse.
64. Clinical Approach in Patients with Chronic Daily Headache
1.Treat medication overuse, if present ( next slide)
2.Select pharmacologic therapies
3.Treat potential underlying pathology Myofascial pain, Physical therapy,
Temporomandibular treatment, Psychiatric comorbidity (antidepressants, anxiolytics)
and Sinus evaluation and treatment etc
4.Limit symptomatic medication use to two days per week (after withdrawal
["detoxification"] is completed).
Recommend use of nonsteroidal anti-inflammatory drugs.
Recommend use of triptans for migraine flares.
Avoid use of medications prone to drug rebound, especially combination analgesics,
caffeine-containing compounds, butalbital products, and narcotics.
5.Consider behavior therapy
Encourage lifestyle management, Regular exercise, Regular meals; no caffeine; migraine
diet
Sleep hygiene
Stress reduction
Biofeedback
Cognitive-behavior therapy
6.Monitor progress (using headache calendar).
65. Treatment of Medication Overuse (Drug Rebound Headache)
1.Withdrawal of symptomatic medications, including caffeine.
A.Gradually taper medications in patients where physiolgic withdrawal is a
concern (i.e., narcotics, butalbital).
B.Use abrupt withdrawal or taper medications in all other patients.
2.Preventive therapy
Any preventive therapy, or combination medicine for headache
3.Transition therapy
Daily migraine-specific therapy
Dihydroergotamine (DHE), intranasal, intramuscular, or intravenous
Long-acting triptan: naratriptan (Amerge) or frovatriptan (Frova)
B.Anti-inflammatory agents
Short course of corticosteroids
Long-acting nonsteroidal anti-inflammatory drugs
4. Rescue therapy, as needed
A.Non-narcotic analgesics: parenteral ketorolac (Toradol)
B.Antiemetics
C.Sedating antihistamines: diphenhydramine (Benadryl) or hydroxyzine (Atarax)
67. Pseudotumor Cerebri
Female to male ratio = 8:1
Females in reproductive age group – common
Obesity and recent weight gain - an important risk
factor.
Pregnancy can precipitate
Commonest complaint – headache. Can cause vision
loss if papilledema is severe. there is no altered level
of alertness, cognitive impairment, or focal neurological
findings that are usually associated with the elevated
ICP
Physical : papilledema
Diagnosis : CT head, Lumbar puncture – elevated
opening pressure. Symptoms improve after LP which is
highly suggestive of BIH. Send CSF to all studies to r/o
other etiologies
68. Treatment
Medical Rx
Weight loss ( goal 1lb/week for 2 months
or longer)
Low sodium diet
Diuretics : Acetalozamide, Furosemide
Surgical Rx:
Optic nerve fenestration
Lumbo-subarachnoid Peritoneal shunting
70. Bells Palsy
Because Bell's palsy is a diagnosis of exclusion, make
every effort to exclude other identifiable causes of facial
paralysis
Consider the following:
Lyme disease : Obtain Lyme disease testing in patients
with acute facial paralysis in endemic areas (Obtain an
ELISA serology for B. burgdorferi in endemic areas if
exposure is likely Obtain confirmation by Western blot
testing if the ELISA result is positive. )
Otologic disease ( chronic otitis media, cholesteatoma)
Neoplasm
Neurologic diseases, such as stroke and MS
71. Bells Palsy – Clues in Hx
Rapidity of onset Onset over more than 3 weeks strongly suggests neoplastic origin
Hearing loss Hearing loss is not usually associated with Bell's palsy Sensorineural
hearing loss suggests Ramsay Hunt syndrome, infectious or neoplastic processes in the
middle ear, cerebella pontine angle affecting the brain stem. Conductive hearing loss
suggests infectious/neoplastic processes within the temporal bone, especially otitis
media/mastoiditis or cholesteatoma
Periauricular pain Mild to moderate pain is common for several days before or after
onset of paralysis. Severe persistent pain suggests Ramsay Hunt syndrome or neoplasm
Bilateral facial palsy Unlikely to be Bell's palsy. Consider Lyme disease, Guillain-Barré,
sarcoidosis, infectious mononucleosis, myasthenia gravis, botulism, acute porphyria,
amyloidosis
Decreased tearing or salivary flow Common in Bell's palsy secondary to involvement of
parasympathetic fibers that travel with the seventh nerve to the lacrimal and salivary
glands
Dysgeusia Common in Bell's palsy due to involvement of the chorda tympani
Duration of paralysis Complete paralysis persisting beyond 6 months. There is always
some recovery from Bell's palsy. Absence of any signs of return of function suggests a
neoplastic etiology
Eye discomfort A common and important problem in Bell's palsy. It is due to poor
corneal hydration and corneal drying secondary to diminished lacrimation and absent blink
reflex
Decreased visual acuity A common and important problem in Bell's palsy. It is due to
poor corneal hydration and corneal drying secondary to diminished lacrimation and absent
blink reflex
72. Bells Palsy – Clues in Physical
A complete ear exam is important to exclude otologic
reasons for seventh nerve paralysis. A maculopapular or
vesicular rash in external ear canal suggests Ramsay
Hunt syndrome
Neurologic exam for segmental focal paralysis Less
than the entire half of the face is involved; e.g.,
involvement of only the mouth or only the eye
Neoplasm of parotid most likely etiology, rather than
Bell's palsy, especially if associated with persistent pain
Neurologic exam for forehead-sparing facial paralysis
Indicates CNS etiology. Consider stroke ( UMN Lesion)
Neurologic exam for balance disturbance Consider
other neurologic disorder or Ramsay Hunt syndrome
rather than Bell's palsy. Ramsay Hunt syndrome
produces balance disturbance by involvement of the
vestibular nerve and/or semicircular canals
73. Treatment
Prescribe a short course of high-dose
prednisone (1 mg/kg·d to 70 mg/d for 7 days,
then tapered) for Bell's palsy as soon as the
diagnosis is made, provided that the patient is
seen within 1 week of the onset of paralysis, and
regardless of the degree of paralysis.
Consider antiviral therapy:
Acyclovir, 200 mg orally, 5 times per day
Valacyclovir, 500 to 1000 mg orally, three times
per day
Famciclovir, 500 mg orally, three times per day
74. Treatment
Manage dry eye aggressively to avoid
ophthalmologic complications Until complete
eye closure and a good blink reflex return, patch
the eye at night, and ensure that the patch itself
does not touch the cornea and abrade it,
Prescribe artificial tears as needed (as often as
every 15 minutes) during the day, and an ocular
lubricant at night.
Refer to physical therapist :
If loss of facial movement is incomplete
After recovery of movement has begun
75. Follow-up
Identify patients who experience atypical
recovery or develop treatment side
effects.
Reevaluate the patient within the first 4 weeks.
Evaluate the patient about every 3 months
thereafter.
Instruct the patient to call immediately if any of
the following develop:
Persistent eye pain
Hearing loss or vertigo
New neurologic signs or symptoms
77. Symptoms n Signs
Sensory loss or paresthesias
Partial or complete monocular loss of vision associated with pain (optic
neuritis)
Blurred vision or impaired color vision
Motor weakness suggesting myelitis syndrome, especially paraparesis
Imbalance due to ataxia or sensory ataxia
Spinal or limb paresthesias elicited by neck flexion (Lhermitte's sign)
Bladder or bowel dysfunction such as urgency, incontinence
Diurnal fatigue
Heat sensitivity, causing worsening of fatigue or neurologic symptoms
Memory loss or other cognitive symptoms
Diplopia
Facial pain consistent with trigeminal neuralgia
Dysarthria or dysphagia
78. M.S Classification
Using the neurologic history, determine if the subtype of MS is:
Relapsing remitting: clinical onset occurs with a “relapse” (“attack”;
“exacerbation”; “flare-up”) of neurologic symptoms or signs that fully
resolve or leave minimal residual deficit
Primary progressive: clinical onset is insidious and worsening of
symptoms occurs gradually over months to years
Secondary progressive: sustained gradual worsening of baseline
status, even between relapses, in patients who initially had
relapsing-remitting disease
Progressive relapsing: a primary progressive onset but the later
establishment of discrete clinical relapses
79.
Obtain:
Brain MRI to assist with MS diagnosis and
to exclude coexisting or other neurologic
disorders
Spinal cord MRI if needed to show
dissemination in space or to exclude a
compressive lesion
80.
Do a lumbar puncture when appropriate based on 2005
Revised McDonald Criteria, usually when an MRI does
not establish dissemination of white matter lesions in
space.
Consider a positive result for purposes of 2005 Revised
McDonald Criteria to be presence of oligoclonal IgG
bands in CSF and not in serum, or an elevated IgG
index.
If MS cannot be confirmed and another diagnosis is not
made, consider serial clinical follow-up examinations and
repeated MRI testing to detect clinical or radiological
changes that may indicate MS.
82. Clinical
(Attacks)
Objective
Lesions
Additional Requirements to Make Diagnosis
2 or more
2 or more
None; additional evidence desirable but must be consistent with MS
2 or more
1
Dissemination in space by MRI or positive CSF and 2 or more MRI lesions
consistent with MS or further clinical attack involving different site
1
2 or more
Dissemination in time by MRI or second clinical attack
1
(monosympto
matic)
1
Dissemination in space by MRI or positive CSF and 2 or more MRI lesions
consistent with MS
AND
Dissemination in time by MRI or second clinical attack
1 (progression
from onset)
1
One year of disease progression (retrospectively or prospectively determined)
AND
Two of the following:
a) Positive brain MRI (nine T2 lesions or four or more T2 lesions with positive
visual evoked potentials)
b) Positive spinal cord MRI (two focal T2 lesions)
c) Positive CSF
Definition of positive MRI—3 out of 4 of the following: 1 gadolinium-enhancing lesion or 9
T2 hyperintense lesions if no gadolinium-enhancing lesion; 1 or more infratentorial
lesions; 1 or more juxtacortical lesions; 3 or more periventricular lesions. Note: A spinal
cord lesion can be considered equivalent to an infratentorial lesion in the brain. Thus, an
enhancing spinal cord lesion is considered to be equivalent to an enhancing brain lesion,
and individual spinal cord lesions can contribute together with individual brain lesions to
reach the required number of T2 lesions.
83. MS - Admission
Hospitalize patients with:
Progressive, rapid, or severe deterioration
in bulbar dysfunction (especially
swallowing), ambulatory function, or level
of consciousness
Medical disorders requiring inpatient
evaluation and therapy, such as infections
or pressure ulcers
84. Treatment
Use an immunomodulatory therapy (βinterferon preparation or glatiramer
acetate) in patients with RRMS to reduce
rates of clinical relapse and prevent new
MRI lesions.
Natalizumab for patients with established
relapsing MS who respond inadequately
to or cannot tolerate other approved MS
immune therapies to delay worsening of
physical disability and reduce the
frequency of clinical exacerbations.
85. Treatment
Consider the use of interferon-β for patients with secondary
progressive MS
Initiate corticosteroid therapy such as methylprednisolone, 1000 mg/d
iv for 3 to 5 days, in patients with exacerbations of MS causing
functional impairment
Treat refractory MS-related fatigue with amantadine, 100 to 200 mg/d;
aspirin, 1300 mg/d; or modafinil, 200 mg/d.
Treat appropriately any other medical disorders or clinical situations
that might worsen MS symptoms or signs such as systemic infection, a
worsening or new medical problem, or medication change
Prescribe an antispasticity drug such as baclofen, tizanidine, or
diazepam for patients with muscle spasms or excessive spasticity
interfering with function.
Prescribe tricyclic antidepressants such as amitriptyline or nortriptyline,
with or without analgesics, for patients with constant epicritic (prickling,
burning) neuropathic pain.
Prescribe anticonvulsant medications such as carbamazepine,
oxcarbazepine, or gabapentin for patients with trigeminal neuralgia or
similar paroxysmal neuropathic pain (shooting, jabbing pain)
associated with MS.
86. Follow-Up
Determine if the patient is experiencing significant and
unacceptable side effects and try to minimize them, for
example:
In patients on corticosteroid therapy, monitor blood pressure
and dietary and blood sugar issues
In patients on interferon therapy,
Monitor for injection-site reactions, skin necrosis,
depression or suicidal ideation, flu-like symptoms, and
obtain laboratory tests every 6 months:
CBC with differential
AST
ALT
Alkaline phosphatase
In patients using any of the β-interferon products, consider
measurement of serum neutralizing antibody status at 12
months and at 24 months after starting therapy or at the
time of a clinical relapse
In patients on immunosuppressive therapy, avoid live vaccines
and unnecessary exposure to viral illnesses
88. Symptoms N Signs
Symptoms
Ptosis or diplopia – esply, new onset
Painless difficulty with repetitive tasks
Painless difficulty in climbing stairs, getting up from a chair, or
walking
Painless difficulty holding arms over head
Dyspnea or difficulty swallowing or chewing
Difficulty holding the head up, or neck muscle soreness
Signs:
Ptosis
Extraocular muscle weakness
Facial weakness
Difficulty swallowing
Effort-related dysarthria dysarthria that worsens with continued
speech.
Proximal muscle weakness
Neck weakness
89.
Diagnosis
Anti-Ach Receptor antibodies are diagnostic.
Anti-AchR antibodies are 50% sensitive and 99 specific
Anti-Musk antibodies are 40% sensitive and 99% specific.
In patients with generalized myasthenia who are
seronegative for anti-AChR antibodies, obtain anti-MuSK
antibodies.
In patients with purely ocular signs of myasthenia who are
negative for anti-Musk and Anti-AchR –ve, diagnose with
pharmacologic and electrophysiologic tests ( Edrophonium
test, EMG) the sensitivity of EMG is 98% and specicficity
is 50-90%.
Consider this diagnosis in presence of classical clinical
features even in the absence of antibodies.
CT chest to r/o thymoma in a pt with newly diagnosed
myasthenia
R/O common co-existent conditions – Hashimato’s
thyroiditis, DM
90. Diagnosis
If all tests show negative results Consider
additional neurophysiologic, serologic,
neuroimaging, CSF, genetic, and muscle
biopsy testing
If no other diagnosis can be made, consider
repeated myasthenia gravis testing in future
91. Differential Diagnosis
MS History or physical findings of autonomic, special sensory (visual
acuity or visual fields, hearing), or sensory involvement is classic in MS and
is not seen in myasthenia
ALS Progressive course, symptoms and signs of both upper and lower
motor neuron disease, asymmetry of weakness early in the disease course,
and fasciculations and lack of involvement of eye movement, sensory or
autonomic, are classic for ALS Unless there is an independent cause of
diplopia or abnormalities of eye movement, the presence of these is
essentially incompatible with ALS Distinction from myasthenia is
particularly difficult for bulbar ALS, but the presence of significant tongue
atrophy and/or fasciculations, or the presence of signs of upper motor
neuron dysfunction (brisk jaw jerk) suggest the diagnosis of motor neuron
disease ( ALS)
Hypothyroidism obtain TFTs
Botulism Descending progressive Paralysis
Eaton-Lambert Syndrome 50%-60% pts have small cell lung ca.
Repetitive stimulation studies cause improvement and this distinguishes
this disorder from myasthenia gravis
92. Treatment
Ach esterase inhibitors for symptoms Pyridostigmine,
Neostigmine
Consider immunotherapy based on the course of an
individual patient treat with one or more
immunosuppressive or immunomodulatory therapies
including:
Corticosteroids such as prednisone or prednisolone
Azathioprine
Mycophenolate mofetil
Cyclosporine
Cyclophosphamide
Plasma exchange
Intravenous immunoglobulin IN MYASTHENIA CRISIS
93. Treatment
Consider modifying the extent of different
types of physical activity including: Heavy
physical effort , Prolonged speaking , Diet
(soft rather than regular) & Prolonged
reading
Recommend thymectomy in all patients
with evidence of thymoma on chest CT or
MRI unless extensive local spread has
already occurred.
94. Drug induced Myasthenia
Penicillmine, Aminoglycosides can cause
drug-induced myasthenia early
diagnosis and discontinuation of the drug
will prevent worsening of symptoms
96. Symptoms
Weakness of gradual onset , Muscle wasting , Muscle twitching
( suggests LMN lesion), Muscle cramps , Clumsiness , Muscle
stiffness ( UMN impairment), Changes in voice or articulation ,
Difficulty swallowing , Difficulty breathing ( bulbar involvement)
Spread of symptoms within one region or to additional regions
defined as cranial, cervical, thoracic, and lumbo-sacral gradual
progression of symptoms suggesting a degenerative disease
Confirm the absence of symptoms that are not typical for ALS,
including:
Predominant sensory symptoms ( favors demyelinating diseases,
neuropathy)
Pain as predominant symptom ( favors radiculopathy, myelopathy)
Bowel or bladder incontinence ( favors cervical myelopathy,
demyelinating diseases)
Cognitive impairment
Ocular muscle weakness ( favors myasthenia)
97. Signs
Muscle wasting and weakness
Fasciculations triggered by muscle contraction or
tapping on a muscle
Spasticity suggests UMN involvement
Hyperreflexia
Hyporeflexia
Brisk jaw jerk/ gag reflex
Evaluate for respiratory muscle weakness looking for
Use of accessory muscles
Paradoxical breathing
Low vocal volume
Lack of breath support
Tachypnea
98. Diagnosis
EMG : Look for electromyographic
evidence of active and chronic
denervation in at least two of four regions
of the CNS ( Brainstem, cervical spinal
cord, thoracic spinal cord, lumbosacral
spinal cord)
Do neuroimaging to r/o other conditions.
99. Treatment
Offer noninvasive ventilatory support to patients with ALS
and respiratory insufficiency.
Monitor respiratory status in ALS patients:
Consider noninvasive ventilatory support:
Do serial FVC or sniff nasal pressure measurements
Ask about symptoms of respiratory insufficiency such as insomnia,
daytime fatigue, morning headaches
Obtain overnight pulse oximetry or polysomnography as needed
In patients with symptoms of respiratory insufficiency
When FVC (sitting or supine) is at or below 50% of predicted normal
If there is evidence of nocturnal hypoventilation (O2 saturation <90%),
even if sitting and supine FVC are not significantly reduced
Consider mechanical insufflation-exsufflation for airway secretion
management in patients with insufficient cough.
Consider a portable suction machine for secretion management.
Physical therapy
Occupational therapy
Speech therapy
100. Treatment
Prescribe riluzole, 50 mg po bid.
Use caution with riluzole and any of its components in patients who:
Have abnormal liver function , Have renal insufficiency , Are elderly ,
Monitor for adverse effects of riluzole treatment, Abdominal pain,
anorexia, diarrhea , Arthralgia, asthenia
Nausea, vomiting
Hypertension, tachycardia (rare)
ALT elevations (rare)
Jaundice (rare)
Neutropenia (rare)
Obtain LFT and blood counts every month for the first 3 months,
then every 3 months for the first year, and periodically thereafter
while the patient is on riluzole.
104. Risk Factors for Dementia
Age
Family history of dementia
History of hypertension
History of head injury
Low education attainment (<10 years)
Alcohol abuse
Current ASA use
Pesticides and fertilizers
Liquid plastics or rubber
? Screen patients Because the incidence of dementia increases
with age, screening has generally been considered for people over
a certain age, usually 60 or 65, but there is currently no evidence on
which to base such recommendations
Screening test – MMSE – Score of 26 or lower is dementia
105. Diagnosis
Ask the patient and the family member about:
Memory loss
Getting lost
Word-finding difficulties
Impaired ADL, such as dressing, grooming, and
housework.
Changes in:
Personality , Mood m Energy , Appetite , Sleep ,
Enjoyment of activities ( Depression is an important
differential diagnosis)
Behavioral changes, including:
General activity level , Eating , Drinking , Sleep , Sex
Neurologic deficits, including:
Gait abnormalities
Falls
Weakness
Clumsiness
Sensory abnormalities
Abnormal movements
Incontinence
106. Diagnosis
Nature and time course of cognitive problems, especially acute vs.
subacute course, or evidence of fluctuating level of consciousness.
The sequence in which the cognitive difficulties and other symptoms
developed should be chronicled
An acute change suggests delirium or a recent CNS event
Fluctuating level of consciousness suggests delirium.
Temporal association with a change in medication suggests a
causal relationship.
Classic Alzheimer disease presents with early loss of short-term
memory, language, and visuospatial abilities, but preserved
personality and normal neurologic exam
Personality change May suggest frontal lobe pathology (e.g,
stroke, tumor, or frontotemporal dementia)
107. Physical exam
Do a mental status exam to evaluate:
Level of alertness
Short- and long-term memory
Orientation
Concentration
Abstract reasoning
Language (naming, vocabulary, fluency, repetition, comprehension)
Visuospatial abilities (clock drawing, design copy)
Cortical-sensory integrative function (neglect, left-right
differentiation, stereognosis, and graphestesia)
Praxis
Mood
Hallucinations or delusions
Apathy
Do a comprehensive neurologic exam, including cranial nerve,
motor, sensory, reflex, and cerebellar function, to look for concurrent
CNS disease.
109. Vascular dementia
Stepwise” deterioration.
Loss of function should be correlated temporally
with cerebrovascular events.
Level of consciousness must be normal to make
the diagnosis.
May also be present in patients with “silent”
strokes, multiple small strokes, or severe diffuse
CVD.
Should be suspected in any patient with
cerebrovascular risk factors, even if a neurologic
exam doesn’t suggest a stroke
110. CJD
Rapid progression
Early age of onset
Prominent myoclonus
Characteristic EEG pattern of triphasic
sharp waves (1-2 Hz)
Diffusion-weighted MRI may be more
sensitive and specific for the diagnosis of
this condition
Poor prognosis
111. HIV Dementia
Seen with advanced HIV
Memory disturbance usually accompanied
by lethargy and social withdrawal, as well
as by motor dysfunction (ataxia,
weakness, and incoordination).
Aphasia, apraxia, and agnosia are rare
112. NPH
Clinical triad of dementia, gait abnormality (slow,
broad-based, impaired turning), and urinary
incontinence.
Dementia is often associated with psychomotor
slowing and apathy.
Dementia and apathy may be the earliest
symptoms
CT scan of head is useful.
If suspicion is high, lumbar puncture with pregait and post-gait monitoring is done.
Ventriculo-peritoneal shunting can be curative in
some patients
113. Delirium vs. Dementia
Altered level of alertness and attention, often in
conjunction with globally impaired cognition.
Onset may be abrupt, and fluctuating level of alertness is
common.
Older patients often appear to have psychomotor
retardation, and may show the full range of mental status
abnormalities, including depressed or elevated mood,
hallucinations, delusions, and agitated behavior
Delirium must be excluded in order to diagnose
dementia.
Making the diagnosis is critical, because it often reflects
a serious systemic disturbance.
Metabolic derangement, medication effects, and
infection are the most common causes
114. Alzheimer’s Disease
Gradual memory loss, preservation of level of consciousness,
inefficiency or impairment in ADL performance may also be present.
May initially become manifest when the patient has lost a significant
source of assistance, for example the loss of a spouse or a
significant change in routine (e.g., moving).
Neurologic signs, such as falls, tremor, weakness, or reflex
abnormalities, are not typical early in the disease course.
As the illness progresses, other cortical deficits, such as aphasia,
apraxia, agnosia, inattention, and left-right confusion will develop.
Seizures are present frequently in advanced disease; their presence
earlier in the course suggests a diagnosis other than Alzheimer
disease.
The presenting symptom to the physician may not be a cognitive
problem.
Often, the earliest presenting symptoms are paranoid delusions or
depression, which upon further investigation turn out to be part of a
dementia
115. Alzheimers - diagnosis
Criteria for clinical diagnosis of PROBABLE Alzheimer's disease
include:
Dementia established by clinical examination and documented by
the Mini-Mental Test, Blessed Dementia Scale, or some similar
examination, and confirmed by neuropsychological tests:
Deficits in two or more areas of cognition
Progressive worsening of memory and other cognitive functions
No disturbance of consciousness
Onset between ages 40 and 90, most often after age 65, and
absence of systemic disorders or other brain diseases that in and of
themselves could account for the progressive deficits in memory
and cognition
116. Drug therapy - Dementia
Use acetylcholinesterase inhibitors to delay cognitive
decline in Alzheimer disease, dementia with Lewy
bodies, and mixed Alzheimer disease and vascular
dementia
Use donepezil, rivastigmine, or galantamine to delay
progression of symptoms in Alzheimer disease,
dementia with Lewy bodies, and mixed Alzheimer
disease and vascular dementia.
Initiate treatment once the diagnosis has been made and
the patient is medically and psychiatrically stable.
Ensure that treatment is continuous and without lengthy
interruptions.
Increase medication doses monthly until target doses
are reached.
117. Drug therapy - Dementia
Do not prescribe high-dose vitamin E routinely to slow
the progression of symptoms in Alzheimer disease.
Use memantine to delay cognitive decline in moderate to
advanced Alzheimer disease and vascular dementia. ,
Begin with 5 mg/d. Increase medication doses weekly
by 5 mg/d until the target dose of 10 mg twice daily is
reached. Add memantine in patients on a stable dose
of a cholinesterase inhibitor, but do not use it as a
substitute
Consider using Ginkgo biloba extract, 120 to 240 mg/d,
in patients with mild to severe Alzheimer disease, but
recognize that there are insufficient data to recommend
its use.
Replace vitamin B12 in patients with evidence of tissue
deficiency of vitamin B12 (elevated methylmalonic acid
and homocysteine).
118. Drug Therapy
Treat psychotic symptoms or behavioral disturbances complicating
dementia with drugs
Consider using one of the following antipsychotic medications in the
treatment of psychotic symptoms (hallucinations and delusions) or
behavioral disturbances (aggression, severe irritability, agitation,
explosiveness) if there is a risk of harm to the patient or others, or if patient
distress is significant and non-drug treatments have been ineffective:
Olanzapine:, Risperidone: Quetiapine, Acetylcholinesterase inhibitors
(donepezil, galantamine, or rivastigmine)
Minimize use of antipsychotics in patients with dementia to the extent
possible by:
Using the lowest effective dose
Restricting use of antipsychotics to patients with hallucinations, delusions,
or agitation, the symptoms for which these medications have proven
efficacy
Treating these symptoms only if they are causing significant problems, such
as distressing the patient or caregiver, jeopardizing a living arrangement, or
necessitating psychiatric hospitalization
Reevaluating the need for continued antipsychotic use on a regular basis
Consider consultation with a geriatric psychiatrist in patients with difficult to
treat symptoms or the development of polypharmacy
119. Drug therapy - Pseudodementia
Treat patients with significant symptoms of depression
with antidepressant drugs: Sertraline, Paroxetine,
citalopram, fluoxetine, venlafaxine
Avoid agents with prominent anticholinergic effects, such
as amitriptyline and imipramine, in patients with
dementia
Maintain treatment at therapeutic doses for at least 6 to
8 weeks before declaring the trial a failure.
Consider referral to a geriatric psychiatrist if one or two
trials of antidepressants (at therapeutic doses given for
at least 6 to 8 weeks) have failed or cannot be tolerated
due to side effects.
Be aware that all of these drugs can cause or
exacerbate delirium.
120. Driving - Dementia
Address the patient's driving ability with the patient and caregiver.
Inquire about motor vehicle accidents or near accidents, and changes in
driving habits or patterns.
Advise patients who already show driving impairment that for their own
safety and the safety of others they must no longer drive.
Advise patients who have received the diagnosis of dementia, but
have not yet shown any difficulties with driving, to undergo a driving
evaluation and to refrain from driving before completion of the
evaluation.
Note that driving evaluations are usually available at the local motor
vehicle agency or hospital departments of occupational therapy.
Follow state law with regard to informing the motor vehicle agency
of a patient's impaired driving ability.
For patients who are able to continue to drive, repeat driving
assessment every 6 months.
