2. Key Areas Determining Sensory Level
3. Key Muscles Determining Motor Level
4. Grading of Muscle Strength
5. Grading of Deep Tendon Reflexes
6. Testing of Cranial Nerves
B. Epilepsy
1. Partial (Focal Epilepsy)
Characterized by focal cortical discharges that provoke seizure sx related to the area of the brain involved. Simple partial seizures do not cause impaired consciousness, whereas complex partial seizures involve an alteration in consciousness.
Etiology
Temporal lobe epilepsy (most common form epilepsy in adults) manifests as a complex partial seizure.
Frequent causes of partial seizures are tumor, stroke, CNS infections (cysticercosis, abscesses), AVMs, traumatic brain injury, cortical malformations, and idiopathic/genetic conditions.Diagnosis
EEG
Ambulatory EEG and/or video EEG if diagnostic uncertaintyH&P
Usually physical/neurologic exam is nl unless the cause is structural abnlity (stroke), wherein neuro exam is consistent with the area of CNS structural damage.
During partial seizures pts are conscious, unless there is spread of the epileptic focus causing secondary generalization and unresponsiveness. A focal seizure can evolve to a generalized tonic clonic seizure. Table 10-4 describes clinical manifestations of different types of focal seizures and areas of the brain involved.Imaging
Head CT to r/o space-occupying lesions. If possible, avoid in children unless an emergency.
Brain MRI with defined epilepsy protocol should be performed if recurrent seizures.Treatment
First unprovoked seizure with nl imaging/EEG/labs generally requires no Rx; recurrent or abnl w/up requires Rx with compliance; avoidance of EtOH and sleep deprivation is essential to prevent recurrence.
No driving is allowed until seizure freedom in accordance w/local laws/regulations (47% seizure free w/monoRx, 67% w/polyRx).
Avoid valproic acid (↑ risk teratogenicity) in women of childbearing age and regardless of antiepileptic drug taken; begin folic acid (1-4 mg/day) to prevent neural tube defects.
Carbamazepine is the traditional initial drug for partial seizures.
FIGURE 10-1 Spinal dermatomes. (From Green GM [ed]: The Harriet Lane Handbook: A Manual for Pediatric House Officers, 12th ed. St. Louis, Mosby–Year Book, 1991.)
TABLE 10-1
Grading of Muscle Strength
| Grade | Description |
| 0 | Absent muscle contraction |
| 1 | Minimal contraction |
| 2 | Active movement with gravity eliminated |
| 3 | Active movement against gravity only |
| 4 | Active movement against gravity and some resistance |
| 5 | Normal muscle strength |
TABLE 10-2
Grading of Deep Tendon Reflexes
| Grade | Description |
| 0 | Absent |
| + | Hypoactive |
| ++ | Normal |
| +++ | Brisker than average |
| ++++ | Hyperactive, often indicative of disease |
TABLE 10-3
Testing of Cranial Nerves
| Cranial Nerves | Action | |
| I | Olfactory | Sense of smell |
| II | Optic | Vision (visual acuity, visual fields, color) |
| III | Oculomotor | Extraocular movement, pupillary constriction (oculomotor), elevation of upper lids, abduction of eye |
| IV | Trochlear | |
| VI | Abducens | |
| V | Trigeminal | Mastication; sensory of forehead, face, and jaw |
| VII | Facial | Facial expression; taste in anterior two thirds of tongue |
| VIII | Acoustic | Hearing and balance |
| IX | Glossopharyngeal | Sensory and motor functions of pharynx and larynx (gag reflex, position of uvula, swallowing) |
| X | Vagus | |
| XI | Accessory | Shrugging of shoulders, movement of head, motor to trapezius, sternocleidomastoid |
| XII | Hypoglossal | Motor control of tongue |
TABLE 10-4
Clinical Manifestations of Different Types of Focal Seizures and Areas of the Brain Involved
| Seizure Type | Areas of Brain Involved | Clinical Expression |
| Somatosensory | Postcentral rolandic; parietal | Contralateral intermittent or prolonged tingling, numbness, sense of movement, desire to move, heat, cold, electric shock; sensation may spread to other body segments |
| Parietal | Contralateral agnosia of a limb, phantom limb, distortion of size or position of body part | |
| Second sensory; supplementary sensory-motor | Ipsilateral or bilateral facial, truncal or limb tingling, numbness, or pain; often involving lips, tongue, fingertips, feet | |
| Motor | Precentral rolandic | Contralateral regional clonic jerking, usually rhythmic, may spread to other body segments in jacksonian motor march; often accompanied by sensory symptoms in same area |
| Supplementary sensory-motor | Bilateral tonic contraction of limbs causing postural changes; may exhibit classic fencing posture; may have speech arrest or vocalization | |
| Frontal | Contralateral head and eye version, salivation, speech arrest or vocalization; may be combined with other motor signs (as above) depending on seizure spread | |
| Auditory | Heschl’s gyrus—auditory cortex in superior temporal lobe | Bilateral or contralateral buzzing, drumming, single tones, muffled sounds |
| Olfactory | Orbitofrontal; mesial temporal cortex | Often described as unpleasant odor |
| Gustatory | Parietal; rolandic operculum; insula; temporal lobe | Often unpleasant taste, acidic, metallic, salty, sweet, smoky |
| Vertiginous | Occipitotemporal-parietal junction; frontal lobe | Sensation of body displacement in various directions |
| Visual | Occipital | Contralateral static, moving, or flashing colored or uncolored lights, shapes, or spots; contralateral or bilateral, partial or complete loss of vision |
| Temporal; occipitotemporal-parietal junction | Formed visual scenes, faces, people, objects, animals | |
| Limbic | Limbic structures: amygdala, hippocampus, cingulum, olfactory cortex, hypothalamus | Autonomic: abdominal rising sensation, nausea, borborygmi, flushing, pallor, piloerection, perspiration, heart rate changes, chest pain, shortness of breath, cephalic sensation, lightheadedness, genital sensation, orgasm Psychic: déjà vu, jamais vu, depersonalization, derealization, dreamlike state, forced memory or forced thinking, fear, elation, sadness, sexual pleasure; hallucinations or illusions of visual, auditory, or olfactory nature |
| Dyscognitive | Usually bilateral involvement of limbic structures (see above) | Previously known as “complex partial seizures,” characterized by a predominant alteration of consciousness or awareness; current definition requires involvement of at least two of five components of cognition: perception, attention, emotion, memory, and executive function |
From Goldman L, Schafer AI (eds): Goldman’s Cecil Medicine, 24th ed. Philadelphia, Saunders, 2012.
Box 10-1 Key Areas Determining Sensory Level
| C2 | Occipital protuberance | T6 | Sixth intercostal space, xiphisternum |
| C3 | Supraclavicular fossa | T7-9 | Intercostal spaces |
| C4 | Top of the acromioclavicular joint | T10 | Umbilicus |
| C5 | Lateral side of the antecubital fossa | T11 | Intercostal space |
| C6 | Thumb | T12 | Inguinal ligament |
| C7 | Middle finger | L1 | Upper anterior thigh |
| C8 | Little finger | L2 | Midanterior thigh |
| T1 | Medial side of the antecubital fossa | L3 | Medial femoral condyle |
| T2 | Apex of the axilla | L4 | Medial malleolus |
| T3 | Third intercostal space | L5 | Dorsum of the foot at the third metatarsophalangeal joint |
| T4 | Fourth intercostal space, nipple line | S1 | Lateral heel |
| T5 | Fifth intercostal space | S2 | Popliteal fossa in the midline |
| S3 | Ischial tuberosity | ||
| S4-5 | Perianal area |
Lamotrigine and levetiracetam are effective and well tolerated.
Antiepileptics (lacosamide, oxcarbazepine, ezogabine) may be used by epilepsy specialists.
Surgery (temporal lobectomy in mesial temporal sclerosis) may be indicated in refractory cases.2. Idiopathic General Epilepsy
Table 10-5 describes a classification and clinical expression of generalized seizures.
Diagnosis
EEG
Ambulatory EEG and/or video EEG if diagnostic uncertaintyTABLE 10-5
Generalized Seizures: Classification and Clinical Expression
| Seizure Type | Subtype | Clinical Expression |
| Absence | Typical | Abrupt cessation of activities, with motionless, blank stare and loss of awareness lasting ≈10 sec; the attack ends suddenly, and pt resumes normal activities immediately |
| Atypical | Longer duration than typical absence, often accompanied by myoclonic, tonic, atonic, and autonomic features as well as automatisms | |
| With myoclonias | Absence with myoclonic components of variable intensity | |
| Myoclonic | Myoclonic | Sudden, brief (<100 msec), shocklike, involuntary, single or multiple contractions of muscle groups of various locations |
| Myoclonic-atonic | A sequence consisting of a myoclonic followed by an atonic phase | |
| Myoclonic-tonic | A sequence consisting of a myoclonic followed by a tonic phase | |
| Tonic | Sustained increase in muscle contraction lasting a few seconds to minutes | |
| Clonic | Prolonged, regularly repetitive contractions involving the same muscle groups at a rate of 2-3 cycles/sec | |
| Atonic | Sudden loss or diminution of muscle tone lasting 1-2 sec, involving head, trunk, jaw, or limb musculature | |
| Tonic-clonic | A sequence consisting of a tonic followed by a clonic phase |
From Goldman L, Schafer AI (eds): Goldman’s Cecil Medicine, 24th ed. Philadelphia, Saunders, 2012.
Labs
Routine blood w/up (CBC, CMP, glucose, electrolytes), urine tox screen
LP recommended if suspicion of meningitisImaging
Head CT scan r/o space-occupying lesions; avoid in children unless a neurologic emergency
MRI of the brain epilepsy protocol performed in all pts with recurrent seizuresTreatment
First unprovoked seizure with nl imaging/EEG/laboratory w/up requires no Rx; recurrent seizures or pts w/abnl w/up require Rx based on type/etiology.
Chronic Rx is indicated for more than two unprovoked seizures or in pts with one seizure with abnl w/up.
Levetiracetam (initial dose 250-500 mg bid, max 1500 mg bid) is an effective and well-tolerated antiepileptic drug for generalized tonic clonic seizures.
Valproic acid (initial dose 10-15 mg/kg/day div bid, max dose 60 mg/kg/day) is better tolerated than topiramate and more efficacious than lamotrigine in pts w/generalized and unclassified epilepsy types; avoid valproic acid (↑ risk teratogenicity) in women of childbearing age and regardless of antiepileptic drug taken; begin folic acid (1-4 mg/day) to prevent neural tube defects.
No driving is allowed until seizure freedom in accordance with local laws and regulations.3. Status Epilepticus
Continuous seizure activity lasting ≥5 min or two or more discrete seizures w/incomplete recovery of consciousness between them.
Diagnosis
Convulsive status epilepticus: Pts are unresponsive w/obvious tonic, clonic, or tonic-clonic extremity movements.
Nonconvulsive status epilepticus varies from complete unresponsiveness w/little or no observable motor activity to confusion and/or repetitive behaviors/automatisms; confirm dx by video EEG monitoring or paradoxical improvement in ms after low-dose benzodiazepine.Management
C. Stroke
1. Transient Ischemic Attack (TIA)
Transient neurologic deficit resulting from focal brain, spinal cord, or retinal ischemia without acute infarction; sx typically <60 min with full function recovery. TIA is a neurologic emergency because 40% pts w/ischemic stroke experience a prior TIA.
FIGURE 10-2 Management algorithm for status epilepticus. CPSE, complex partial status epilepticus; GSCE, generalized convulsive status epilepticus, NCSE, nonconvulsive status epilepticus; SE, status epilepticus. (From Vincent JL, Abraham E, Moore FA, et al [eds]: Textbook of Critical Care, 6th ed. Philadelphia, Saunders, 2011.)
Box 10-3 Characteristics of Carotid Artery Syndrome
Ipsilateral monocular vision loss (amaurosis fugax); the pt often feels as if “a shade” has come down over one eye
Episodic contralateral arm, leg, and face paresis and paresthesias
Slurred speech and transient aphasia
Ipsilateral headache of vascular type
Carotid bruit may be present over the carotid bifurcation
Microemboli, hemorrhages, and exudates may be noted in the ipsilateral retina
Box 10-4 Characteristics of Vertebrobasilar Artery Syndrome
Binocular visual disturbances (blurred vision, diplopia, and total blindness)
Vertigo, N/V, and tinnitus
Sudden loss of postural tone of all four extremities (drop attacks) w/no loss of consciousness
Slurred speech, ataxia, and numbness around lips or face
Etiology
Cardioembolic
Large-vessel atherothrombotic disease
Lacunar disease
Hypoperfusion w/fixed arterial stenosis
Hypercoagulable statesDiagnosis
H&P
Imaging
Head CT, brain MRI, MRA
Carotid Doppler, echo, ECG
Telemetry for hospitalized ptsLabs
CBC w/Plt, PT, PTT
Glucose, lipid profile, ESR
CXR; other tests dictated by suspected etiologyTreatment
Depends on etiology. Table 10-6 describes the characteristics of thrombosis vs embolism. The ABCD2 score can help stratify pts who are at highest risk of subsequent stroke after TIA (Table 10-7). Consider hospital admission for pts with ABCD2 score >3 or those with transient monocular blindness.
Acute anticoagulation is indicated for new-onset AF and atherothrombotic carotid disease causing recurrent transient neurologic sx, especially before carotid endarterectomy (CEA) or carotid stenting. It is also considered for basilar artery thrombosis, given concern for progression to brainstem stroke w/high morbidity and mortality.
Antiplatelet therapy should be used to reduce the risk of recurrent TIAs or subsequent stroke. Three antiplatelet agents are commonly used in stroke prevention: aspirin, aspirin/dipyridamole, and clopidogrel. All are reasonable choices, but practitioners should consider their individual pt’s comorbidities when selecting an antiplatelet agent.
Chronic therapy should be aimed at modifying the four major risk factors: BP control, control of dyslipidemia, control of blood sugar, and smoking cessation.TABLE 10-6
Characteristics of Thrombosis and Embolism
| Thrombosis | Embolism | |
| Onset of sx | Progression of sx during hours to days | Very rapid (seconds) |
| Hx of previous TIA | Common | Uncommon |
| Time of presentation | Often during night hours while pt is sleeping Classically, pt awakens w/a slight neurologic deficit that gradually progresses in a stepwise fashion |
Pt is usually awake and involved in some type of activity |
| Predisposing factors | Atherosclerosis, HTN, diabetes, arteritis, vasculitis, hypotension, trauma to head and neck | AF, mitral stenosis and regurgitation, endocarditis, mitral valve prolapse |
TABLE 10-7
ABCD2 Risk of Stroke After a TIA
| Score (points) | |
| Age ≥60 yr | 1 |
| BP: ≥140 mm Hg systolic or 90 mm Hg diastolic | 1 |
| Clinical features Unilateral weakness Speech disturbance without weakness |
2 1 |
| Duration of TIA ≥60 min 10-59 min |
2 1 |
| Presence of diabetes mellitus | 1 |
| Two-day risk of stroke is 4.1% with a score 4-5 and 8.1% with a score 6-7. | |
Modified from Ballinger A: Kumar & Clark’s Essentials of Clinical Medicine, 6th ed. Edinburgh, Saunders, 2012.
2. Ischemic Stroke
Rapid onset of neurologic deficit involving a certain vascular territory secondary to thrombosis or embolism
Diagnosis
H&P
Imaging
Immediate CT of the head without contrast or MRI of the brain with stroke protocol to rule out hemorrhage and, if possible, to assess the extent of stroke. CT of brain: area of ↓ density; initial CT scan may be nl because the infarct may not be evident for 2 to 3 days afterward.
TABLE 10-8
Selected Stroke Syndromes
| Artery Involved | Neurologic Deficit |
| Middle cerebral artery | Hemiplegia (UEs and face usually more involved than LEs) Hemianesthesia (hemisensory loss) Hemianopia (homonymous) Aphasia (if dominant hemisphere is involved) |
| Anterior cerebral artery | Hemiplegia (LEs more involved than UEs and face) Primitive reflexes (e.g., grasp and suck) Urinary incontinence |
| Vertebral and basilar arteries | Ipsilateral cranial nerve findings, cerebellar findings Contralateral (or bilateral) sensory or motor deficits |
| Deep penetrating branches of major cerebral arteries (lacunar infarction) | Usually seen in elderly pts with HTN and diabetic pts Four characteristic syndromes are possible: 1. Pure motor hemiplegia (66%)
2. Dysarthria—clumsy hand syndrome (20%)
3. Pure sensory stroke (10%)
4. Ataxic hemiplegia syndrome w/pyramidal tract signs
|
Treatment
IV TPA is the only medical therapy approved by the U.S. FDA for the treatment of acute ischemic stroke.
The time window for administration is ≤3 hr of symptom onset.
The protocol is weight based, with 90 mg being the maximum allowable dose.
The risk of brain hemorrhage with IV TPA is ≈5% in pts w/stroke.
Multimodal therapy (i.e., thrombectomy and intra-arterial TPA) is sometimes performed.
Endovascular treatment may be performed for select cases in which IV TPA has failed to recanalize an occluded artery.
Endovascular intervention may be an option for pts w/systemic contraindications to IV TPA.Box 10-5 Inclusion and Exclusion Criteria for IV TPA
Inclusion Criteria
1. Ischemic stroke onset is within 3 hours of drug administration.
2. Measurable deficit is noted on NIH Stroke Scale examination.
3. Pt’s CT does not show hemorrhage or nonstroke cause of deficit.
4. Pt’s is >18 years old.
Exclusion Criteria (Absolute)
1. Pt’s symptoms are minor or rapidly improving.
2. Pt had seizure at onset of stroke.
3. Pt has had another stroke or serious head trauma within the past 3 months.
4. Pt had major surgery within the last 14 days.
5. Pt has known hx of intracranial hemorrhage.
6. Pt has sustained SBP >185 mm Hg.
7. Pt has sustained DBP >110 mm Hg.
8. Aggressive treatment is necessary to lower the pt’s BP.
9. Pt has symptoms suggestive of SAH.
10. Pt has had gastrointestinal or urinary tract hemorrhage within the last 21 days.
11. Pt has had arterial puncture at noncompressible site within the last 7 days.
12. Pt has received heparin with the last 48 hours and has elevated PTT.
13. Pt’s PT is >15 sec.
14. Pt’s Plt count is <100,000 μL.
15. Pt’s serum glucose is <50 or >400 mg/dL.
Exclusion Criteria (Relative)
1. Pt has a large stroke with NIH Stroke Scale score >22.
2. Pt’s CT shows evidence of large MCA territory infarction (i.e., sulcal effacement or blurring of gray-white junction in greater than one third of MCA territory).
NIH, National Institutes of Health.
Modified from Vincent JL, Abraham E, Moore FA, et al (eds): Textbook of Critical Care, 6th ed. Philadelphia, Saunders, 2011.
Endovascular intervention is useful only for large, accessible thrombi. Therefore, if a pt w/stroke is a candidate for IV TPA, then he or she should probably receive IV TPA.
Antiplatelet therapy: Beginning oral or feeding tube administration of aspirin (325 mg/day) ≤48 hours of stroke onset is advised. This will decrease the likelihood of a repeat ischemic stroke. Another oral antiplatelet regimen approved for secondary stroke prophylaxis (e.g., clopidogrel, aspirin plus extended-release dipyridamole) will also suffice and may be superior in the long term.
↑ BP is common during acute stroke, and it often subsides without specific Rx. In general, HTN is not treated acutely unless it is extremely high (e.g., >220 mm Hg SBP); unless there is evidence of organ damage caused by the HTN; or unless thrombolysis is being considered, in which case BP needs to ↓ (if it can be safely accomplished) to ∼185/110 mm Hg. It is risky to ↓ BP severely the presence of acute ischemic stroke. A 15% to 25% decrease over the first 24 hours is recommended.3. Acute Hemorrhagic Stroke
a. Intracranial hemorrhage
Neurologic deficit secondary to intracerebral hemorrhage (17% of all strokes)
Etiology
HTN (50%-60%)
Cerebral amyloid angiopathy (10%)
Hemorrhagic infarcts (10%)
Use of anticoagulants and fibrinolytic agents (10%)
Brain tumors (5%)
Vascular malformations (5%)Diagnosis
H&P
Signs of ↑ ICP (e.g., bradycardia, ↓ RR, third nerve palsy)
FIGURE 10-3 Circle of Willis. ACOM, anterior communicating artery; MCA, middle cerebral artery; PCA, posterior cerebral artery; PCOM, posterior communicating artery. (From Weissleder R, Wittenberg J, Harisinghani M, Chen JW [eds]: Primer of Diagnostic Imaging, 5th ed. St. Louis, Mosby, 2011.)
Imaging
Immediate: CT scanning of the head without contrast is highly sensitive for hemorrhage (area of hemorrhagic infarct appears as a zone of ↑ density).
MRI of the brain with a gradient echo sequence is also highly sensitive for hemorrhage, including intracerebral microhemorrhages that may not be visible with CT scanning.Treatment
Surgery should be performed promptly for cases of cerebellar hemorrhage of >3 cm when the pt is deteriorating clinically or showing brainstem edema or hydrocephalus.
Surgery for lobar or deep brain clots may be considered for select cases, although the level of evidence for efficacy is not high.
Pneumatic compression devices should be applied to help prevent DVT.
Early mobilization for rehabilitation is desirable.TABLE 10-9
Localizing Signs in Pts w/Intracerebral Hemorrhage
| Location of Intracerebral Hemorrhage | Common Neurologic Signs | Examples |
| Putamen | Both eyes deviating conjugately to the side of the lesion (away from hemiparesis) Pupils normal in size and reacting normally Contralateral hemiplegia present Hemisensory defect noted |
Left putaminal hemorrhage |
| Thalamus | Both eyes deviating downward and looking at the nose Impairment of vertical eye movements present Pupils small (≈2 mm) and nonreactive Contralateral hemisensory loss present |
Thalamic hemorrhage |
| Pons | Both eyes in midposition No doll’s-eye movements Pupils pinpoint but reactive (use magnifying glass) Coma common Flaccid quadriplegia noted |
Pontine hemorrhage |
| Cerebellum | Ipsilateral paresis of conjugate gaze (inability to look toward side of lesion) Pupils normal in size and reacting normally Inability to stand or to walk Vertigo and dysarthria present |
Cerebellar hemorrhage |
HTN: BP should be quickly lowered by 15% and then gradually and safely brought to the individual pt’s target range. In theory, this may diminish expansion of the hematoma. Recommended guidelines for Rx of HTN in pts w/spontaneous hemorrhage are described in Box 10-6.
Hyperglycemia: A high blood glucose level predicts a worse outcome. Markedly elevated glucose levels should be lowered to <300 mg/dL.
Seizures: If seizures occur, they should be treated aggressively, including with IV medications, if needed.
↑ ICP: This condition should be treated with a graded approach, which may include the elevation of the head of the bed, analgesia/sedation, hyperventilation, and osmotic therapy.
Antipyretics should be administered for cases that involve fever; in addition, the cause of the fever should be sought.
Protamine sulfate is used to treat cases of heparin-induced intracerebral hemorrhage.
Vitamin K is given for warfarin-associated intracerebral hemorrhage. In addition, recombinant factor VIIa and fresh frozen plasma are sometimes used.
Recommendations for thrombolytic-associated intracerebral hemorrhage treatment include the consideration of the infusion of Plts and cryoprecipitate.b. Subarachnoid Hemorrhage (SAH)
Diagnosis
H&P
Abrupt onset of severe occipital or generalized headache that radiates into the posterior neck region and is worsened by neck and head movements; often described as “the worst headache” of the pt’s life
Restlessness, vomiting, diminished level of consciousness, syncope
Focal neurologic signs usually are absent.
Level of consciousness varies from nl to deeply comatose.
Fever and nuchal rigidity are present or usually develop within 24 hr.
Fundi may show papilledema or retinal hemorrhage.
Cranial nerve abnlities may be noted (e.g., pupillary dilation secondary to oculomotor nerve dysfunction).
HTN may be present and can lead to an incorrect dx of primary hypertensive emergency.
Tachycardia and irregular heartbeat may be present (≤91% of pts w/SAH have cardiac arrhythmias).Imaging and Labs
CT of brain is (+) in >95% of cases, especially during the acute phase (i.e., 24-48 hr) after the onset of bleeding.
A CT angiogram or a cerebral angiogram is imperative for determining the origin of the SAH. Angiography may also be extremely useful because it may offer a therapeutic benefit via the coiling of the aneurysm.
Basic labs should include CBC, chemistry panel, PT, PTT, Plt count, troponin.
LP is a very important part of the w/up, especially because 3% of pts with normal CT scans show evidence of hemorrhage on LP. An RBC count of >100,000/m3 strongly suggests SAH. If RBC counts ↓ between the first and fourth tubes, then the tap is most likely traumatic. The presence of xanthochromia or bilirubin in the CSF is a sign of SAH.Treatment
Management of SAH varies w/the pt’s clinical status (Table 10-10), as well as the location (see Fig. 10-3) and surgical accessibility of the aneurysm.TABLE 10-10
Glasgow Coma Scale∗
| Eyes | Motor | Verbal |
| 1. None | 1. None | 1. None |
| 2. To pain | 2. Abnl extension | 2. Incomprehensible (groaning) |
| 3. To speech | 3. Abnl flexion | 3. Inappropriate |
| 4. Spontaneous | 4. Flexion (withdrawal) | 4. Disoriented, confused |
| 5. Localizing | 5. Oriented | |
| 6. Obeying commands |
∗ The best score for each response should be documented and communicated in the format described above. Assessment of the best motor score is based on the best response of the arms. For use in individual pts, separate description of the three components of the GCS is strongly recommended. For purposes of classification, the total GCS can be calculated by adding the best score obtained in each category. The GCS should be annotated to indicate confounding factors: T signifies an intubated pt; S, sedation; P, neuromuscular blockade.
From Vincent JL, Abraham E, Moore FA, et al (eds): Textbook of Critical Care, 6th ed. Philadelphia, Saunders, 2011.
Pts with a depressed level of consciousness may need to be intubated and mechanically ventilated in an ICU setting.
A lumbar drain or ventriculostomy is required should the pt develop hydrocephalus and ↑ ICP.
Initial management strategies are geared toward stabilizing the pt and preventing recurrent hemorrhage and hydrocephalus.
Tight BP control is paramount. This can be done with the use of drips (e.g., nitroprusside) or PRN medications. An SBP 120 to 150 mm Hg is recommended.
After an aneurysm has been identified, measures to secure it should be undertaken; this can be done by either clipping or coiling the aneurysm. Clipping consists of placing a clip around the neck of the aneurysm and is performed via intra-arterial angiography; it consists of deploying platinum coils inside the aneurysm to cause thrombosis of the aneurysmal sac.
Pain control is performed with the use of short-acting and less-sedating medications (e.g., codeine, low-dose morphine).
Seizures occur in ≤3% of pts during the acute phase; however, the use of prophylactic antiepileptics is still controversial.
Vasospasm, which typically begins around day 3 after the hemorrhage and reaches a peak on day 6 to 8, is the leading cause of death and disability after aneurysm rupture. Nimodipine has been shown to improve outcomes if it is administered between days 4 and 21 after the hemorrhage, even if it does not significantly reduce the amount of vasospasm detected on angiography. After vasospasm develops, “triple H” therapy—to achieve Hypertension, Hypervolemia, and Hemodilution—is used in an attempt to provide adequate cerebral perfusion.4. Sinus Venous Thrombosis
Etiology
Staphylococcus aureus (50%-60%), Streptococcus (second leading cause), gram(−) rods/anaerobes; sphenoid sinusitis (most common site)Diagnosis
H&P
Ptosis, proptosis
Chemosis
CN palsies (III, IV, V (VI and VII), VI); VI is most common
Sensory deficits of the ophthalmic/maxillary branch of the fifth nerve are common.Labs
CBC, ESR, blood/sinus cultures (identify infectious primary source)
LP necessary to r/o meningitisImaging
MRV, MRI w/gadolinium including MR angiographyTreatment
Rx should take into account the primary source of infection, as well as possible associated complications, such as brain abscess, meningitis, or subdural empyema.
Broad-spectrum IV abx are used as empiric Rx until a definite pathogen is found. Rx should include a penicillinase-resistant PCN at maximum dose plus a third- or fourth-generation ceph:• Nafcillin (or oxacillin) 2 g IV q4h plus either ceftriaxone (2 g q12h) or cefepime (2 g q6h)
• Metronidazole 500 mg IV q6h should be added if anaerobic bacterial infection is suspected (dental or sinus infection).
• Vancomycin (1 g q12h w/nl renal function) may be substituted for nafcillin if significant concern exists for infection by MRSA or resistant Streptococcus pneumoniae.
Anticoagulation w/heparin: controversial. Cerebral infarction or ICH should first be ruled out by non–contrast-enhanced CT scan before initiation of heparin Rx. Current recommendation is for early heparinization in pts w/unilateral CST to prevent clot propagation and to ↑ the incidence of septic emboli. Warfarin Rx should be avoided in the acute phase of the illness but should ultimately be instituted to achieve an INR of 2 to 3 and continued until the infection, sx, and signs of CST have resolved or significantly improved.
Steroid Rx: controversial but may prove helpful in ↓ cranial nerve dysfunction or when progression to pituitary insufficiency occurs. Corticosteroids should be instituted only after appropriate abx coverage. Dexamethasone 10 mg q6h is the Rx of choice.
Emergency surgical drainage w/sphenoidotomy: indicated if the primary site of infection is thought to be the sphenoid sinus.
All pts w/CST are usually treated w/prolonged courses (3-4 wk) of IV abx. If there is evidence of complications such as intracranial suppuration, 6 to 8 wk of total Rx may be warranted.
All pts should be monitored for signs of complicated infection, continued sepsis, or septic emboli while abx Rx is being administered.5. Stroke Prevention: Asymptomatic Carotid Stenosis
Carotid stenosis is narrowing of the arterial lumen within the carotid artery.
Etiology
Atherosclerosis (most common)
Aneurysm
Arteritis
Carotid dissection
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