Transcript 10 and 11 - Neurology

Neurology
NEUROLOGY
CHAPTER 24
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Symptoms: Headache (HA)
Acute:
Age > 50 years.
Rapid onset and severe intensity.
Fever.
Trauma.
Vision changes.
Past medical history of hypertension or HIV infection.
Hypertension.
Neurologic findings (mental status changes, motor or sensory
deficits).
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Headches
Chronic:
Migraine (pulsating or throbbing),
Tension (tightness or pressure ), or
Depression
Tumor, head injury, cervical spondylosis, dental or
ocular disease, TM joint dysfunction, sinusitis,
hypertension
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Headaches
 Sharp and lancinating – neuralgic
 Ocular/periorbital-icepick like pain- migraine/cluster
headaches
 Dull and steady- tumor
 Cough aggravated in brain tumors
 Severe headache in a previously well patient: rule outsub arachnoid hemorrhage/ meningitis
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Headaches
 Cranial MRI or CT scan required if:
 New onset in middle or later life
 Progressive
 Disturb the sleep/related to exertion
 Associated with neurological deficit
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Tension Headaches
 Poor concentration
 Vague non specific symptoms
 Vise-like, worse on emotional stress/noise/
glare and occurs almost daily
 Intense around back of the neck & head
 May respond to Tylenol/ or migraine medicine
 Relaxation therapy/Massage/Hot baths/
Biofeedback/?Botox
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Depression HA
 Worse on waking up
 Associated depressive symptoms
 Antidepressants/Psychiatric help
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Migraine HA
 Headache, usually pulsatile/dull/throbbing.
 Nausea, vomiting, photophobia, and
phonophobia are common
 Transient neurologic symptoms (commonly
visual) preceding headache of classic
migraine.
 No preceding aura is common.
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Migraine
Related to serotonin (5-HT)
Trigeminal trigger
Episodic lateralized throbbing headache
Late teen/early adult onset
Anorexia/Nausea/Vomiting
Visual/Auditory disturbances- gradual build up, last
several hours
 External Carotid artery system dilation/pulsation
 Focal neurological signs/symptoms due to initial
constriction of ICA
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Migraine
 Visual: common field defects
 luminous visual hallucinations such as stars,
sparks, unformed light flashes, geometric patterns,
or zigzags of light
 Aphasia/numbness/tingling/clumsiness
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Migraine
 FH+
 Factors- emotional stress, lack/excess sleep, missed
meals, specific food items (chocolate, alcohol),
menses, pill
 ‘Basilar artery’ migraine- blindness/visual field
defects initially and later- tinnitus/perioral tingling
and transient loss of consciousness/ confusion
followed by throbbing occipital HA, nausea/vomiting
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Migraine: Treatment
 AVOID! Factors
 Prophylactic treatment:
aspirin/brufen/allieve
 Ergot + caffeine (vasoconstrictor)
 Serotonin blockerSumatriptan/Zolimtriptan
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Table 24–1. Prophylactic treatment of migraine.
Drug
Usual Adult
Daily Dose
Common Side Effects
Propranolol
80–240 mg
Fatigue, lassitude, depression, insomnia, nausea,
vomiting, constipation.
Amitriptyline
10–150 mg
Sedation, dry mouth, constipation, weight gain,
blurred vision, edema, hypotension, urinary retention.
Imipramine
10–150 mg
Similar to those of amitriptyline (above).
Sertraline
50–200 mg
Anxiety, insomnia, sweating, tremor, gastrointestinal disturbances.
Fluoxetine
20–60 mg
Similar to those of sertraline (above).
Cyproheptadine
12–20 mg
Sedation, dry mouth, epigastric discomfort,
gastrointestinal disturbances.
Clonidine
0.2–0.6 mg
Dry mouth, drowsiness, sedation, headache,
constipation.
Verapamil2
80–160 mg
Headache, hypotension, flushing, edema, constipation.
May aggravate atrioventricular nodal heart block
and congestive heart failure.
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Cluster Headache
(Migrainous Neuralgia)
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Predominantly middle-aged men
?Vascular/?serotonin
No FH+
Unilateral periorbital pain withipsilateral nasal congestion,
rhinorrhea,
lacrimation,
redness of the eye, and
Horner's syndrome
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Horner syndrome
 Results from an interruption of the sympathetic
nerve supply to the eye, and is characterized by
the classic triad:
 1 Miosis (ie, constricted pupil)
 2 Partial ptosis and
 3 Loss of hemifacial sweating (ie, anhidrosis)
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Cluster Headache
(Migrainous Neuralgia)
 AT night (wakeup)
 Lasts <2hrs
 Spontaneous remission
 ?alcohol trigger/ glare/food
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THERAPY
 Oxygen (acute attack)
 Oxygen (8 L/min for 10 min or 100% by mask) may abort the headache if used early.
 Mechanism of action is unknown.
 Sumatriptan
 Most studied of the triptans in cluster headache.
 Subcutaneous injections can be effective, in large part, due to the rapidity of onset.
 No evidence suggests that they are effective orally.
 Dihydroergotamine
 Can be abortive agent
 IV/IM; self-injections
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Posttraumatic Headache
 Closed head injury
 Worsen over the ensuing weeks, and then gradually
subsides
 Disequilibrium, enhanced by postural change or head
movement
 Impaired memory, poor concentration, emotional
instability, and increased irritability
 Tests not helpful, Treatment difficult
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?
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TRIGEMINAL NERVE
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Trigeminal Neuralgia
 Brief episodes of stabbing facial pain.
 Pain is in the territory of the second and
third division of the trigeminal nerve.
 Pain exacerbated by touch
 Middle and later life (F>M)
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Trigeminal Neuralgia
 Sudden lancinating facial pain occur
 commonly arise near one side of the mouth and shoot toward
the ear, eye, or nostril on that side
 Trigger-touch, movement, drafts, and eating
 Pain become more frequent, remissions become shorter and
less common, and a dull ache may persist between the
episodes of stabbing pain
 Confined to the distribution of the trigeminal nerve (usually
the second or third division
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Trigeminal Neuralgia
 Young patient presenting with trigeminal neuralgia,
multiple sclerosis
 Tests-evoked potential testing and examination of
cerebrospinal fluid may be corroborative
 Treatment- carbamazepine (Tegretol)/ Baclofen/
Gabapentin
 Nerve ablation
 Structural cause for the neuralgia (despite normal
findings on CT scans, MRI, or arteriograms) -surgery
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TCM Diagnoses and
Acupuncture Treatments
 Etiology & Pathology:
 Exterior –WIND-COLD
Invasion
 Interior – LV/ST FIRE
 Interior – YIN DEFICIENCY
w/empty fire rising
 Differentiation:
 Wind-Cold Invasion
 Signs & Symptoms:
 Acute onset, severe pain
for a few seconds to a few
minutes several times/day
 Exterior signs, runny nose,
tearing
 Tongue: Thin white coat
 Pulse: Tight, floating
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LV/ST Fire
Signs & Symptoms:
Severe pain w/irritability
Internal heat signs, thirst,
constipation
Tongue:Yellow, dry coat
Pulse: Wiry
Yin Deficiency w/empty heat
rising
Signs & Symptoms:
Pain is more insidious, gradual,
comes and goes, malar flush,
soreness in lumbar area
Tongue: Red w/no coat
Pulse: Thin, fast
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Treatment Points
 For pain in the supraorbital region:
 Local: Taiyang
 GB14/ UB2
 Distal: TH5 / LI4
 For pain in the maxillary region:
 Local: ST2 / SI 18 / LI 20
 Distal: LI4
 For pain in the mandibular region:
 Local: ST6 / ST 7
 Extra point 1 cun lateral to CV24
 Distal: LI4
 Wind-Cold : Add GB 20
 LV/ST Fire: Add LV3, possibly LV2, ST44
 Yin Deficiency : Add KD6, SP6
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Glossopharyngeal Neuralgia
 Occurs in the throat, about the tonsillar
fossa, and sometimes deep in the ear and
at the back of the tongue
 Precipitated by swallowing, chewing,
talking, or yawning
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Postherpetic Neuralgia
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 15% of patients who develop shingles
suffer from postherpetic neuralgia
High risk: elderly and involvement of
Ophthalmic (I)
division
Incidence of postherpetic neuralgia may be reduced by the
treatment of shingles with oral acyclovir or famciclovir (?)
Corticosteroids do not help (?)
Zoster vaccine for elderly (?)
 ZOSTAVAX® [Zoster Vaccine Live (Oka/Merck)]
 Carbamazepine/TCA/Lidocaine (local)
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Epilepsy
 Recurrent seizures.
 Characteristic electroencephalographic
changes accompany seizures.
 Mental status abnormalities or focal
neurologic symptoms may persist for hours
postictally
 Seizure is a transient disturbance of cerebral
function
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Epilepsy
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Usually begin between 5 and 20
Congenital abnormalities and perinatal injuries
Alcohol withdrawal/hypo or hyper glycemia
Trauma (within 2 years following the injury)
Tumors-especially important cause of seizures in middle and
later life , must be excluded by appropriate imaging studies in
all patients with onset of seizures after 30 years of age
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RED FLAGS!Epilepsy
 Epilepsy-Old age –
 Vascular diseases
 Alzheimer's disease
 Infectious disease-
 AIDS
∆bacterial meningitis or herpes encephalitis
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Seizure Type
Key Features
I: Partial seizures
Involvement of only restricted part of brain; may
become secondarily generalized
Other Associated Features
1) Simple partial
Consciousness preserved
May be manifested by focal motor, sensory, or
autonomic symptoms
2) Complex partial
Consciousness impaired
Above symptoms may precede, accompany, or
follow
II: Generalized seizures
1) Absence (petit mal)
Diffuse involvement of brain at onset
Consciousness impaired briefly; patient often unaware of
attacks
May be clonic, tonic, or atonic components (i.e.,
loss of postural tone); autonomic components
(e.g., enuresis); or accompanying automatisms
Almost always begin in childhood and
frequently cease by age 20
2) Atypical absences
3) Myoclonic seizures
4) Tonic-clonic (grand mal)
May be more gradual onset and termination than typical
absence
More marked changes in tone may occur
Single or multiple myoclonic jerks
Tonic phase: Sudden loss of consciousness, with rigidity
and arrest of respiration, lasting < 1 minute
May be accompanied by tongue biting,
incontinence, or aspiration; commonly
followed by postictal confusion variable in
duration
Clonic phase: Jerking occurs, usually for
< 2–3 minutes
Flaccid coma: Variable duration
III:
Status epilepticus
Repeated seizures without recovery between them; a
fixed and enduring epileptic condition lasting 30 minutes
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Tests
 Imaging? new onset of seizures after the age of 20
years,
 A chest radiograph should also be obtained
in such patients, since the lungs are a
common site for primary or secondary
neoplasms.
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Tests
 EEG
 CBC
 Blood glucose
 BUN, Creatinine
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DD
 TIAs
 Rage attacks
 Panic attacks
 Syncope
 Cardiac arrhythmias
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Treatment
 goal of preventing further attacks and is
usually continued until there have been no
seizures for at least 3 years
 report to the state department of public
health any patients with seizures or other
episodic disturbances of consciousness
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Generalized tonic-clonic (grand mal) or
partial (focal) seizures
 Phenytoin -Dilantin®,
 Carbamazepine-Tegretol®
 Valproic Acid, Depakene®
 Gabapentin Neurontin®
 Topiramate Topamax®
 Ethosuximide Zarontin®
 Clonazepam Klonopin®
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 Monitoring serum drug levels has led to
major advances in the management of
seizure disorders
 Surgical treatment
 Vagal nerve stimulation
 Status epilepticus is a medical emergency
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Sensory Disturbances
1.Peripheral Nerve
2.Nerve roots
3.One limb
4.One half of the
body
5.Distal:
‘glove & stocking’
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Weakness & Paralysis :
1Upper/Lower motor
neuron
2Spinal roots
3Plexus
4Peripheral nerves
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UMN
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Muscle groups involved
Spasticity
Brisk DTRs
Babinski’s Sign present
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LMN
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Muscle wasting
Falccid weak muscle
Loss of DTRs
Babinski’s sign absent
Fasciculations present
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Transient Ischemic Attacks: TIAs
 Focal neurologic deficit of acute onset.
 Clinical deficit resolves completely
within 24 hours.
 Risk factors for vascular disease often
present.
 Increased in patients with
hypertension or diabetes
 Risk of stroke is highest in the month
after a transient ischemic attack
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TIA: Causes
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Emboli- from Carotids
Cardiac- atrial fibrillation, post infarction
Cervical spondylitis
Subclavian steal syndrome: bruit in the
supraclavicular fossa, unequal radial pulses, and a
difference of 20 mm Hg or more between the
systolic blood pressures in the arms
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TIA symptoms:
 Abrupt onset –within minutes
 Rapid recovery
 Carotid territory - Weakness and heaviness
of the contralateral arm, leg, or face, singly
or in any combination.
Slowness of movement, dysphasia, or
monocular visual loss in the eye contralateral
to affected limbs.
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Vertebrobasilar ischemic attacks
Vertigo, ataxia, diplopia,
dysarthria, dimness or blurring
of vision, perioral numbness and
paresthesias, and weakness or
sensory complaints on one,
both, or alternating sides of the
body
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TIA risks:
 Carotid ischemic attacks are more
liable than vertebrobasilar ischemic
attacks to be followed by stroke
 Stroke risk is greater in patients older
than 60 years, in diabetics, or after
transient ischemic attacks that last
longer than 10 minutes and with
symptoms or signs of weakness,
speech impairment, or gait
disturbance.
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Imaging Tests
 CT scans
 Carotid duplex US
 Aretirography
 MRI angio less sensitive than
conventional
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Lab Tests
 Assessment for: hypertension, heart
disease, hematologic disorders, diabetes
mellitus, hyperlipidemia, and peripheral
vascular disease
 CBC/ Lipids, Cholesterol, Homocysteine/
ECG/ CXR/ Echo/ Holter
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Treatment
 Carotid artery surgery
 Preventive- Stop smoking/ treat underlying
disease/
 If embolic- anticoagulants
 ?antiplatelet drugs- aspirin 325 mg/ or
Plavix ®75 mg (clopidogrel)
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Strokes
 Sudden onset of characteristic neurologic
deficit.
 Patient often has history of hypertension,
diabetes mellitus, valvular heart disease, or
atherosclerosis.
 Distinctive neurologic signs reflect the
region of the brain involved.
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Four Main Types of Strokes
 Ischemic
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1 Cerebral thrombosis (61% of all strokes, excluding transient
ischemic strokes), a blood clot (thrombus) forms in an artery that
supplies blood to the brain
2 Cerebral embolism (24% of all strokes), a clot (embolus)
develops in a blood vessel and is carried through the bloodstream
and becomes lodged in a brain artery
Thrombosis and embolism account for about 85% of strokes.
These strokes are ischemic, or caused by blood clots, which result
in insufficient blood circulation.
 Hemorrhagic
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3 Subarachnoid hemorrhage (3% of all strokes), a blood
vessel on the surface of the brain ruptures, causing bleeding into
the space between the brain and skull
4 Cerebral hemorrhage (9% of all strokes), an artery in the
brain ruptures, causing bleeding into the surrounding brain tissue
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Strokes
Third leading cause of death
 Risk factors:
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hypertension
diabetes
hyperlipidemia
cigarette smoking
cardiac disease
AIDS
recreational drug abuse
heavy alcohol consumption
family history of stroke
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Stroke Classification:
 Infarcts- 85%
 Thrombotic}
 Embolic
}
 Hemorrhagic } 12%
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Lacunar Infarcts
 Small (<5mm) basal ganglia/ pons/
cerebellum/anterior limb of internal
capsule
 Common in poorly controlled HTN or
diabetics
 Recovery good: takes 4-6 weeks
 Contralateral pure motor or pure
sensory deficit
 Ipsilateral ataxia with crural paresis
and
 Dysarthria with clumsiness of the hand
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Stroke Assessment
Abrupt onset
?bruit present
1. Anterior
2. Middle
3. Posterior
4. Vertebrobasilar
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6.
7.
8.
9.
Anterior cerebral artery
Anterior communicating artery
Internal carotid artery
Posterior communicating artery
Middle cerebral artery
Posterior cerebral artery
Superior cerebellar artery
Basilar artery
Anterior inferior cerebellar artery
1.
2.
3.
4.
5.
6.
Internal carotid artery
Vertebral artery
Cavernous sinus
Carotid canal
Anterior cerebral artery
Posterior cerebral artery
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Anterior
cerebral artery
Weakness and
sensory loss in contralateral
leg
Mild arm weakness
Grasp reflex +
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Middle cerebral
artery
 Contralateral hemiplegia
 Hemisensory loss, and
 Homonymous hemianopia (i.e., bilaterally
symmetric loss of vision in half of the visual
fields), with the eyes deviated to the side of
the lesion
 Global aphasia if dominant hemisphere
involved
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Posterior
cerebral artery
 Receptive (Wernicke's)
aphasia and
 A homonymous visual field defect
 Confusional state
 Dressing apraxia* and
 Constructional and spatial deficits
*The
inability to execute a voluntary motor movement despite being
able to demonstrate normal muscle function. Apraxia is not related to
a lack of understanding or to any kind of physical paralysis but is
caused by a problem in the cortex of the brain.
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Vertebrobasilar artery
Involuntary movements
and
Alexia*
*Loss of the ability to read
or understand the written word
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Posterior inferior
cerebellar artery
Ipsilateral spinothalamic sensory loss
involving:
The face, ninth and tenth cranial
nerve lesions
Limb ataxia and numbness, and
Horner's syndrome
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Superior
cerebellar artery
 The contralateral
 spinothalamic loss also involves the face
 And ipsilateral the face, ninth and tenth cranial nerve
lesions
 limb ataxia and numbness, and
 Horner's syndrome
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Anterior inferior
cerebellar artery
ipsilateral spinothalamic sensory
loss involving the face, usually in
conjunction with ipsilateral facial
weakness and deafness
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THROMBOSIS OF ICA
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Therapy for thrombotic strokes
 T-pa* initiation within 3 hours after stroke
onset, and the prognosis therefore depends
on the time that elapses before arrival at
the hospital
“CLOT BUSTERS”
* Tissue-plasminogen activator Retiplase
RETAVASE®
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Intracerebral Hemorrhage
 Usually due to hypertension
 Most frequently in the basal ganglia and less
commonly in the pons, thalamus, cerebellum, and
cerebral white matter
 Common in- advancing age and male sex
 Consciousness is initially lost or impaired in about
one-half of patients
 Vomiting
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Tests/ Treatment
 CT scanning (superior to MRI) for this
 Management: generally conservative and
supportive,
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Subarachnoid Hemorrhage
 Sudden severe headache.
 Signs of meningeal
irritation usually present.
 Obtundation is common.
 Focal deficits frequently
absent
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SUBARACHNOID HEMORRHAGE
 5% and 10% of strokes are due to
subarachnoid hemorrhage
 sudden headache of a severity never
experienced previously by the patient
 May lead to coma and death
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Brain Tumors
 Frontal lobe: intellectual decline,
slowing of mental activity, personality
changes, and contralateral grasp
reflexes.
 Expressive aphasia.
 Anosmia may also occur as a
consequence of pressure on the
olfactory nerve.
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Temporal lobe
 olfactory or gustatory hallucinations
 licking or smacking of the lips, and some
impairment of external awareness
 depersonalization, emotional changes,
behavioral disturbances, sensations of déjà vu
or jamais vu, micropsia or macropsia
 dysnomia and receptive aphasia (L)
 musical notes and melodies (R)
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Parietal lobe
 Sensory loss- postural / tactile
discrimination
 appreciation of shape, size, weight, and
texture is impaired
 Objects placed in the hand may not be
recognized (astereognosis)
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Parietal lobe
 Gerstmann's syndrome
 (a combination of-
Alexia
Agraphia
Acalculia
Agnosia (right-left confusion, and finger)
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Occipital lobe
 Field defect
 Visual agnosia both for objects and for
colors
 Color perception, prosopagnosia (inability
to identify a familiar face)
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Brainstem and cerebellar
 Cranial nerve palsies, ataxia,
incoordination, nystagmus, and pyramidal
and sensory deficits in the limbs on one or
both sides.
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Tests for Tumors
 CT scans
 MRI scans
 EEG
 Treatment:: ? Surgery/ anticonvulsants
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Neurofibromatosis
 Multiple hyperpigmented
macules (café au lait spots )
(chromosome 17 )
 Eighth nerve tumors
(chromosome 22 )
 Mobile nodules
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PARKISNOSNS PATHOLOGY
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Parkinsonism
 Tremor, rigidity, bradykinesia, progressive
postural instability.
 Seborrhea of skin quite common.
 Mild intellectual deterioration may occur
 Begins most often between 45 and 65
years of age.
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Parkinsonism
 Familial
 Toxins-manganese, carbon disulfide, carbon
monoxide poisoning
 Degeneration of the dopaminergic
nigrostriatal system
 Imbalance of dopamine and acetylcholine
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Parkinsonism
 Tremor- most conspicuous at rest, less severe during
voluntary activity
 Rigidity,
 Bradykinesia, and
 Postural instability
 Immobile face with widened palpebral fissures,
infrequent blinking, and a certain fixity of facial
expression.
 Seborrhea of the scalp and face is common
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Parkinsonism
 Sustained blink response (Myerson's sign)
 Saliva drooling from the mouth
 Gait itself is characterized by small
shuffling steps and a loss of the normal
automatic arm swing
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Drugs for Parkinsonism
 Amantadine
 Cogentin
Artane
Levodopa /Sinimet
 Selegeline
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Huntington's Disease
 Gradual onset and progression of chorea
and dementia or behavioral change.
 Family history of the disorder.
 Responsible gene identified on chromosome
4 (AD)
 chorea and dementia
 5 per 100,000
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Huntington’s
 Onset is usually between 30 and 50 years
 Fatal outcome within 15–20 years
 Abnormal movements or intellectual changes,
but ultimately both occur
 CT scanning usually demonstrates cerebral
atrophy and atrophy of the caudate nucleus in
established cases (reduced glucose utilization )
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Huntington's Disease
 No cure for Huntington's
 Relative under activity of neurons
containing gamma-aminobutyric acid
(GABA) and acetylcholine or a relative
overactivity of dopaminergic neurons.
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Restless Leg Syndrome: RLS
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RLS affects about 10-15% of the general population
M=F
Often unrecognized or misdiagnosed.
Many patients are not diagnosed until 10-20 years after
symptom onset.
It may begin at any age, even as early as infancy
Middle-aged or older are affected severely .
Symptoms progress over time in about two thirds of
patients and may be severe enough to be disabling.
"pins and needles," an "internal itch," or "a “creeping” or
“crawling” sensation.
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RLS DIAGNOSTIC CRITERIA
1. A compelling urge to move the limbs, usually associated with
paresthesias/dysesthesias
2. Motor restlessness, as seen in activities such as floor pacing,
tossing and turning in bed, and rubbing the legs
3. Symptoms worse or exclusively present at rest (ie, lying, sitting)
with variable and temporary relief on activity
4. Circadian variation of symptoms, which are present in the evening
and at night. Often, symptoms are relieved after 5:00 am. In more
severe cases, symptoms can be present throughout the day
without circadian variation.
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DD for RLS
 Iron deficiency and peripheral neuropathy
 Folate or magnesium deficiency
 Polyneuropathy (either idiopathic or caused by alcohol
abuse)
 Amyloidosis
 Diabetes mellitus
 Lumbosacral radiculopathy
 Lyme disease
 Rheumatoid arthritis, Sjögren syndrome
 Uremia or
 Vitamin B-12 deficiency
 Affects 25-40% of pregnant women
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Restless Legs Syndrome
 Idiopathic disorder or in relation to pregnancy, irondeficiency anemia, peripheral neuropathy, or periodic
leg movements of sleep
 ? hereditary
 Irresistible urge to move the limbs, especially during
periods of relaxation. Disturbed nocturnal sleep and
excessive daytime somnolences may result.
 clonazepam. Levodopa
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Gilles de la Tourette's Syndrome
Multiple motor (80%) and phonic tics. (20%)
Symptoms begin before age 21 years.
Tics occur frequently for at least 1 year.
Tics vary in number, frequency, and nature over time.
Onset: ages of 2 and 15.
Motor tics :face, head, and shoulders (e.g., sniffing, blinking,
frowning, shoulder shrugging, head thrusting,
 Phonic tics: grunts, barks, hisses, throat-clearing, coughs,
obscene speech
 Obsessive-compulsive behaviors
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