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Page 117


In patients seen soon after the onset of neurologic
symptoms, an attempt should be made to reperfuse
the ischemic brain if a brain-supplying large artery is
occluded and if a large portion of the brain area sup-
plied by that artery is not already infarcted. Brain and
vascular imaging can show the location and extent of
brain infarction and vascular occlusion. Reperfusion
can be attempted using intravenous thrombolysis or
by intra-arterial interventions using thrombolysis or
mechanical means. Cerebral blood flow should be

maximized by optimizing blood pressure and fluid

Prevention of further brain ischemia often in-
volves using an antithrombotic agent. Heparin, and
later warfarin, is used in patients with cardiac srcin
embolization (mostly due to atrial fibrillation and
myocardial infarction) and in some patients with ar-
terial dissection and acute large artery occlusions.
Antiplatelet drugs—aspirin, clopidogrel, a combina-
tion of aspirin and modified-release dipyridamole, or
cilostazole—are given to patients with lacunar in-
farction and nonocclusive atherosclerotic lesions.

Control of stroke risk factors (hypertension, dia-
betes, obesity, hyperlipidemia, smoking) is accom-
plished by attention to lifestyle behavior, nutri-
tion, and exercise, and by prescribing appropriate

Chapter 14 / Vascular Disease • 101101

Figure 14-5 •Figure 14-5 •Bright signal is seen on a diffusion-weighted MR

image (DWI), indicating a recent infarction.

• The course of development of symptoms and re-

sults of brain imaging should allow separation of

ischemia from hemorrhage, and in case of ischemia,

identification of the most likely stroke mechanism:

thrombosis, embolism, or systemic hypoperfusion.

• Cardiac and brain and vascular imaging should

identify the cause of the stroke.


• Acute and preventive treatments should be tai-

lored to the individual patient.

• Maximizing cerebral blood flow to ischemic regions

can be facilitated by opening blocked arteries

chemically or mechanically, and by increasing

blood flow in collateral vessels.



Bleeding inside the skull can be divided into subarach-
noid, intracerebral, epidural, and subdural hemor-
rhages. The latter two types of hemorrhages are al-
most always traumatic and are discussed in Chapter
17. Intracerebral hemorrhage (ICH) and subarachnoid
hemorrhage (SAH) have different causes, clinical find-
ings, and management.


SAH is predominantly caused by bleeding from an
aneurym located along the circle of Willis. The most
common sites of cerebral aneurysms are shown in
Figure 14-6. When blood under arterial pressure is
suddenly released into the space around the brain,
patients develop sudden headache, often vomit, and
have a temporary interruption in behavior. If the re-
sultant increase in intracranial pressure is severe,
coma or death may ensue. An example of an SAH is
shown in Figure 14-7.

Page 118

102102 • Blueprints Neurology

Figure 14-7 •Figure 14-7 •Subarachnoid hemorrhage. A CT scan showing

extensive subarachnoid blood within the sulci of the brain.

The most bleeding is seen in the left frontal region.

are neurologic signs related to the region of the
bleeding. Bleeding into the putamen-internal cap-
sule region might cause early contralateral limb
weakness, while cerebellar bleeding would cause
gait instability. ICHs continue to grow until the
pressure around the lesion equals that in the
hematoma or the hematoma drains into the ventric-
ular system or the pial surface.

Hypertension is the commonest cause of ICH. The
commonest locations for hypertensive ICH are: basal
ganglia-internal capsule, caudate nucleus, thalamus,
pons, and cerebellum. Trauma, cerebral amyloid

angiopathy, vascular malformations, and bleeding
diatheses (especially with patients on anticoagulants)
are other common causes.


There is a variety of congenital and acquired vascular
anomalies (angiomas) that have the potential to
bleed, either within the brain (ICH) or around it.

Arteriovenous malformations (AVMs) contain arter-
ies that empty into arterialized veins. These lesions
contain no recognizable normal capillary bed, but ab-
normal gliotic parenchyma can be found between the
component vessels. The most common brain vascular
malformations are developmental venous anomalies
(DVAs) that are composed of anomalous veins usu-

ally separated by morphologically normal brain
parenchyma. One or more large central draining veins
are usually conspicuous and may be dilated into a
varix or varices. Cavernous angiomas consist of a rel-
atively compact mass of sinusoidal vessels close to-
gether, without intervening brain parenchyma. The
lesions are well encapsulated. Telangiectasias are di-
lated capillaries with intervening brain parenchyma.
Brain and vascular imaging can distinguish between
these subtypes.

• AVMs, DVAs, cavernous angiomas, and telangiecta-

sis are different types of malformations, each with

differing clinical findings and management.

• Medical therapy, surgery, interventional oblitera-

tion, and radiotherapy are all used in treating brain

vascular malformations.


Figure 14-6 •Figure 14-6 •Common sites of aneurysm in the circle of Willis.
(Reproduced with permission from Ginsberg L. Lecture Notes: Neurology,

8th ed. Oxford: Blackwell Publishing, 2005:87.)

Treatment is aimed at prevention of rebleeding
and vasoconstriction that often follows SAH.
Aneurysms can be clipped surgically or “coiled” by in-
terventional techniques. Calcium-channel blockers
are often used to minimize vasoconstriction and de-
layed brain ischemia.


ICH describes bleeding directly into brain paren-
chyma. In contrast to SAH, the earliest symptoms

Page 234

218 •• IndexIndex

Quetiapine, 177

Radiculopathy, 44, 126

Radiographic studies
of acute disseminated
encephalomyelitis, 144
of coma and altered consciousness,
of seizures, 107

RAPD. See Relative afferent pupillary

Reading, disorders of, 80

Reflex syncope, 56, 56t

Reflexes, 4t, 8, 8 f, 23–24, 23t, 37, 44,44t, 180t

Relative afferent pupillary defect
(RAPD), 30

REM sleep-related parasomnias, 94

Reserpine, 112

Respiratory muscle weakness, 170–171

Restless legs syndrome (RLS), 93

Rigidity, 7, 111

Riluzole, 157

Risperidone, 89, 177

Rivastigmine, 87, 87t

RLS. See Restless legs syndrome

Romberg sign, 9

Roots. See Nerve roots

Ropinirole, 93, 112, 113t

Saccades, 37

SAH. See Subarachnoid hemorrhage
Sarcoidosis, neuropathy of, 125–126

SCAs. See Spinocerebellar ataxias

Schwannoma, 136

Scintillating scotoma, 70

SE. See Status epilepticus

Secondarily generalized seizure, 103

Secondary brain tumors, 138, 138 f

Secondary headache disorders, 11, 69,

Sedatives, 68

Seizures, 27, 103–110, 104 f –105 f, 106t,
108t, 109 f, 121, 131, 149–150

Selective serotonin reuptake inhibitors, 94

Selegiline, 91, 112, 114t

Sellar tumors, 137–138, 137 f

Sensory ataxia, 61t, 62

Sensory loss, 51 f, 52–53, 52t, 154
Sensory nerve action potential
(SNAP), 16

Sensory system, 4t, 8–9, 24, 48–53,
49 f –50 f

Sexual dysfunction, 68

Sildenafil, 68

Simple partial seizures, 103

Single-photon emission computed
tomography (SPECT), 14, 146

Sixth nerve. See Abducens

Skeletal muscle, disorders of, 169–177,
170t, 177t

Skew deviation, 36

Slapping gait, 61t, 62

SLE. See Systemic lupus erythematosus

Sleep apnea, 95

Sleep disorders, 92–95, 93 f
Sleep-phase disorders, 93

Sleep-wake transition disorders, 94–95

SMA. See Spinal muscular atrophies

SNAP. See Sensory nerve action

Sneddon syndrome, 129

Sodium oxalate, 94

Spastic bladder, 65, 65t, 67t

Spastic gait, 61

Spasticity, 7, 157

SPECT. See Single-photon emission
computed tomography

Speech. See Communication disorders

Spina bifida, 158

Spinal cord
anatomy of, 152, 153 f
compression of, 153–154

disorders of, 47, 47 f, 152–158, 155 f
incontinence and, 66
sensory loss in, 52t, 53
subacute combined degeneration
of, 128
transection of, 154

Spinal epidural abscess, 147

Spinal muscular atrophies (SMA),

Spine, tuberculosis of, 148

Spinocerebellar ataxias (SCAs), 60

Spinothalamic tract, 48, 49 f, 152,
153 f, 154

Spongiform encephalopathies, 90

Status epilepticus (SE), 109, 109 f

Steele-Richardson-Olszewski syndrome.
See Progressive supranuclear palsy

Steroid myopathy, 176

Steroids, 71, 73, 114, 126–127, 137,
143, 150, 157, 162–163, 171, 175–176

Stiff-person syndrome, 113–114

Strabismus, 35t

Stress incontinence, 65, 67t

Stroke, 96–102, 100 f –102 f
with antiphospholipid syndrome,129
aphasia with, 79
embolism, 98
incontinence with, 66
of spinal cord, 156
systemic hypoperfusion, 99
thrombosis, 98

Stupor, 21

Subacute combined degeneration of
spinal cord, 128

Subarachnoid hemorrhage (SAH), 72,
101–102, 102 f

Subcortical aphasia, 78t, 80
Subdural hematoma, 119–120, 120 f

Subfalcine herniation, 122

Supranuclear eye movements, 37

Suprasellar tumors, 137–138, 137 f

Supraspinal disease, incontinence with, 66

Sympathetic nervous systems,
neuropathies of, 166

Syncope, 55–57, 56 f, 56t

Syphilis, 33

Syringomyelia, 154–155, 155 f

Syrinx, 154–155, 155 f, 158

Systemic disorders, 124–130, 125t
alcohol and nutritional disorders,
127–128, 127t
antiphospholipid syndrome, 129
central pontine myelinolysis, 130
diabetes mellitus, 45, 126–127,

126b, 164–165, 164t hepatic encephalopathy, 124–125
neurosarcoidosis, 125–126
systemic lupus erythematosus,
thyroid disease, 129–130, 130b

Systemic hypoperfusion, 99

Systemic lupus erythematosus (SLE),

TAC. See Trigeminal autonomic

Tacrine, 87t

Tacrolimus, 144

Taenia solium, 150

Tardive dyskinesia, 112

TCD. See Transcranial Doppler

Telangiectasias, 102

Temozolomide, 133–134
Temporal arteritis, 73

Tension-type headache, 71

Tetrabenazine, 112

Theophylline, 115b

Page 235

IndexIndex •• 219

Thiamine, 22, 22 f, 128

Third nerve. See Oculomotor nerve

Thrombosis, 98

Thyroid disease, nervous system and,
129–130, 130b

Thyrotoxic myopathy, 176

Tiagabine, 108t

Tics, 117

Tizanidine, 143

Tolcapone, 113t

Tolterodine, 67t

Tonic pupil. See Adie’s pupil

Tonic seizure, 104

Topiramate, 108t, 115

Tourette’s syndrome, 117

Toxin-induced myopathies,
176–177, 177t

Toxoplasmosis, 150–151

Transcranial Doppler sonography
(TCD), 14

Transection, of spinal cord, 154

Transtentorial herniation, 122

Transverse myelitis, 140

to head, 119–123, 120 f –121 f, 122t
to spinal cord, 154, 157

Treatment. See specific diseases and
disorders, e.g., Acute bacterial
meningitis, Alzheimer disease

Tremor, 111, 114–115, 115b

Triamcinolone, 176

Tricyclic antidepressants, 67t, 69, 71, 74,
94, 165, 177

Trientine, 118

Trigeminal autonomic cephalgias
(TAC), 71

Trigeminal nerve, 48

Trigeminal neuralgia, 73–74

Trihexyphenidyl, 113t

Triptans, 71

Trochlear nerve, 35

Tropia, 35t, 37

Tropical spastic paraparesis, 157

Tuberculous infection, 147–148

of central nervous system,
131–138, 132t
pituitary, 137–138, 137 f
primary brain tumors, 131–138,
132t, 134 f –137 f
secondary (metastatic) brain tumors,
138, 138 f

Uhthoff phenomenon, 141

UMN. See Upper motor neuron
Uncal herniation, 122

Upper motor neuron (UMN), 46 f, 47

Uremic neuropathy, 165

Urge incontinence, 65, 67t

Urinary dysfunction, 63–68, 64 f, 65t, 67t

Vacuolar myelopathy, 151

Vagus nerve stimulation, 108

Valproate, 116

Valproic acid, 108t, 110

Vardenafil, 68

Vascular disease, 96–102, 97 f –98 f,
100 f –102 f . See also Stroke

dementia with, 84, 87t, 88,
100 f –102 f, 101–102
with diabetes mellitus, 127
incontinence with, 66
of spinal cord, 156

Vascular imaging, 14, 14 f

Vascular malformations, 102

Vasodilators, 56

Venlafaxine, 94

Verapamil, 71

Vertebro-basilar circulation. See Posterior

Vertigo, 54–55, 55b, 56t

Vestibular neuronitis, 54–55

Vestibulo-ocular reflex (VOR), 37

Vincristine, 134, 162b, 166

Viral infections, 149

Vision, assessment of, 30

Visual loss, 29–31, 30 f, 31b, 31t

Vitamin B12 deficiency, 91, 128

Vitamin deficiency syndromes, 127t

Vitamin E, 87, 87t

von Hippel-Lindau disease, 137, 185t

VOR. See Vestibulo-ocular reflex

Waddling gait, 61–62, 61t

Walking. See Gait

Wallerian degeneration, 159

Warfarin, 87t, 101
WD. See Wilson disease

Weakness, 16–17, 40–47, 41 f, 43t –44t,
45 f –47 f, 169–177, 170t

channelopathies, 172, 174
distal myopathies, 175
dystrophinopathies, 172–173
Emery-Dreifuss muscular dystrophy,
170t, 174
endocrine and drug- or toxin-
induced myopathies, 176–177, 177t
inflammatory myopathies, 175–176
Lambert-Eaton myasthenic
syndrome, 169, 170t, 171–172
limb-girdle muscular dystrophy,
170t, 172–173
mitochondrial myopathies, 175
myasthenia gravis, 169–171, 170t
myotonic dystrophy, 170t,

neuroleptic malignant syndrome,112, 177
patterns of, 41–47, 43t, 45 f –47 f

Wernicke’s aphasia, 27, 78 f, 78t, 79

Wernicke’s encephalopathy, 128

Wilson disease (WD), 117–118

Writing, disorders of, 80

Xanthochromia, 10

X-ray, of spinal cord disorders, 158

Zidovudine (AZT), 91, 177t

Zonisamide, 108t

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