Neuro Interna

Question 1

Infective endocarditis

Answer 1

Infective endocarditis can lead to a variety of neurologic
complications due to septic cerebral embolization, including but
not limited to ischemic stroke (most common), intracranial
hemorrhage (most often due to hemorrhagic conversion of an
ischemic infarct), subarachnoid hemorrhage, cerebral abscess,
meningoencephalitis, and seizures. Headaches and encephalopathy
also occur, often as a symptom of the latter complications.
Septic cerebral emboli can lead to mycotic aneurysms by causing
intraluminal arterial wall necrosis (due to arteritis) and destruction
of the adventitia and muscularis with subsequent dilatation.
Mycotic aneurysms are usually located at distal arterial
bifurcations and are best detected by conventional cerebral
angiography.

Neurologic complications occur in both patients with native and
prosthetic valve endocarditis in a similar proportion. In those with
prosthetic valves, those with mechanical valves may have more
complications than those with bioprosthetic valves. Left-sided
endocarditis is associated with higher risk of neurologic
complications as compared to right-sided cases.

Question 2

Tatalaksana infection endocarditis

Answer 2

Because of increased risk of hemorrhagic conversion,
anticoagulation in patients with ischemic stroke due to infective
endocarditis is warranted only in specific cases such as in patients
with mechanical valves.

Question 3

Komplikasi Neurologis sickle cell anemia (Hemoglobin [Hb] SS disease

Answer 3

Ischemic stroke is more common than intracerebral hemorrhage in
patients with sickle cell anemia (Hemoglobin [Hb] SS disease). The
pathophysiology of ischemic strokes in these patients is not
completely understood, with sickling and increased viscosity likely
playing a significant role. However, large-vessel intracranial
stenosis and/or occlusions are also frequently encountered,
sometimes with Moyamoya-like appearance.
Neurologic complications of Hb SS disease include ischemic
stroke, intracranial hemorrhage, cranial neuropathies, spinal cord
infarction (although rare), intracranial aneurysm formation with
subarachnoid hemorrhage, ischemic optic neuropathy, optic
atrophy, seizures, and headaches. Ischemic stroke is more common
in children with Hb SS disease than in adults. In children,
transcranial Doppler ultrasonography should be periodically
performed, and when elevated velocities are detected, blood
transfusion (or exchange transfusion) have been shown to reduce
the risk of ischemic stroke. Blood transfusions or exchange
transfusions are used with the goal of reducing the percentage of
hemoglobin S, therefore reducing the percentage of red blood cells
that can sickle.

Question 4

plasma cell dyscrasias

Answer 4

plasma cell dyscrasias include Waldenström
macroglobulinemia (smoldering or symptomatic), monoclonal
gammopathy of unknown significance (MGUS), multiple myeloma
(smoldering or symptomatic), plasmacytomas (bone and
extramedullary), primary amyloidosis, idiopathic Bence Jones
proteinuria, among others.

Question 5

Neurologic complications plasma cell dyscrasias

Answer 5

Neurologic complications of the plasma cell dyscrasias include a
wide spectrum of manifestations. Neuropathy in patients with
plasma cell dyscrasias can be due to infiltration of the peripheral
nervous system by abnormal cells, amyloidosis, or a paraneoplastic
syndrome.
Infiltration of peripheral nerves would typically cause a
sensorimotor predominantly axonal neuropathy. Infiltration of
vertebral bodies can be extensive enough to lead to nerve root as
well as spinal cord compression. Patients with plasma cell
dyscrasias may develop encephalopathy due to hypercalcemia,
hyperviscosity syndrome (due to hypergammaglobulinemia), and
CNS infections, which such patients are prone to due to their
immunocompromised state. Direct CNS involvement in plasma cell
dyscrasias can occur but is relatively rare. POEMS syndrome
(plasma cell dyscrasia with polyneuropathy, organomegaly,
endocrinopathy, monoclonal gammopathy, and skin changes) is a
constellation of abnormalities seen in some patients with plasma
cell dyscrasias, particularly plasmacytoma, and not with leukemias.

Question 6

Hiponatremi

Answer 6

Hyponatremia typically causes more severe neurologic
symptoms when it develops rapidly, but symptoms can also occur
with chronic hyponatremia. A nonspecific encephalopathy is the
most frequent manifestation. Seizures can occur with acute
hyponatremia, usually with serum sodium levels of 115 mEq/L or
less. Correction of serum sodium levels is the mainstay of
treatment of hyponatremia-associated seizures, but care must be
taken not to correct serum sodium levels too rapidly, given the risk
of central pontine myelinolysis. The rate
of correction of hyponatremia should be no more than 12 mEq/L
per day, or 0.5 mEq/L per hour. CNS manifestations of
hypernatremia typically occur with serum sodium concentrations
higher than 160 mEq/L and include encephalopathy, seizures, and
in severe cases coma.

Question 7

hypothyroidism

Answer 7

In a patient presenting with cognitive dysfunction, apathy, and
hypersomnolence, hypothyroidism is a diagnostic possibility, and
serum thyroid-stimulating hormone (TSH) level should be tested.
Thyroid function should be assessed in all patients presenting with
cognitive dysfunction, but particularly older adults. Congenital hypothyroidism is the most treatable cause of mental
retardation. Untreated, it leads to cretinism, which is manifested
by cognitive dysfunction, gait dysfunction, and hearing loss. The
most common cause is dysgenesis of the thyroid, but severe
maternal iodine deficiency also can lead to it.
Both hypothyroidism and hyperthyroidism can lead to myopathy.
Serum creatine kinase level is typically elevated. Gait dysfunction
in patients with thyroid disorders could be due to cerebellar ataxia,
myopathy, neuropathy, or a combination of these.

Pseudomyotonia, or a delay in muscle relaxation following
elicitation of deep tendon reflex, is a feature of hypothyroidism.

Question 8

hyperthyroidism

Answer 8

Tremor is almost universally present in patients with untreated
hyperthyroidism. It is typically a postural, high-frequency tremor
that is thought to result from increased β-adrenergic activity. Other
abnormal movements seen in patients with hyperthyroidism
include parkinsonism, dyskinesia, chorea, and myoclonus.

Pseudomyotonia, or a delay in muscle relaxation following
elicitation of deep tendon reflex, is a feature of hypothyroidism.

Question 9

Thyroid eye disease

Answer 9

Thyroid eye disease in patients with Graves’ disease results from
an immune-mediated increase in connective tissue of the orbit.
Manifestations include proptosis, extraocular muscle enlargement
with restricted movement, optic nerve compression, and ocular
neuromyotonia. Restricted upward gaze is the most common
extraocular abnormality seen in patients with thyroid eye disease,
but impaired abduction, adduction, and downward gaze also occur.
Eyelid retraction in patients with Graves’ disease may be due to
overactivation of Muller muscle (a sympathetically innervated
muscle) or eyelid fibrosis.

Question 10

Myxedema coma

Answer 10

Myxedema coma, due to severe untreated hypothyroidism,
typically occurs in older adults and is often precipitated by
intercurrent illnesses. Clinical features include hypothermia and
encephalopathy. Seizures occur in some patients.
Patients with hypothyroidism may develop diffuse peripheral
neuropathy with both axonal and/or demyelinating features and
entrapment neuropathy, most commonly carpal tunnel syndrome,resulting from deposition of mucopolysaccharides.
Other neurologic manifestations of thyroid disease include both
obstructive and central sleep apnea, headache, and hearing
impairment with tinnitus.

Question 11

Cushing
disease

Answer 11

Cushing
disease, which results from hypercortisolism in the setting of an
ACTH-secreting pituitary adenoma. Neurologic manifestations of
Cushing disease include headache, proximal myopathy, cognitive
dysfunction, and behavioral changes, with psychosis in severe
cases.
The bitemporal hemianopia is a clue to a
compressive lesion of the optic chiasm, distinguishing Cushing
disease from Cushing syndrome, which can result from cortisolsecreting tumors or from ectopic ACTH production as can occur
with paraneoplastic syndromes or other causes.

Question 12

osteopetrosis

Answer 12

osteopetrosis, a sclerosing
bone disorder characterized by pathologically increased bone mass
due to impaired bone resorption by osteoclasts. It is caused by a
mutation in an ATPase or a chloride channel. Autosomal dominant
and recessive forms exist, each differing in their age at
presentation and clinical manifestations. Some of the younger-onset
forms are severe. The majority of patients are asymptomatic, but
symptoms may include bone pain, joint deformities, secondary
osteoarthritis, and fractures. Many adults with osteopetrosis are
asymptomatic, but cranial neuropathies may occur because of skull
thickening with subsequent narrowing of cranial nerve (CN)
foramina in the base of the skull. The most commonly involved
CNs are CN II (in some cases leading to optic atrophy with
blindness), VII, and VIII, leading to irreversible hearing loss, as in
this patient. Elevated serum alkaline phosphatase level is a clue to
this diagnosis. The olfactory nerve is also commonly involved.

Question 13

Paget disease

Answer 13

Paget disease results from excessive
bone turnover and abnormal compensatory bone formation. It is
often asymptomatic and diagnosed incidentally, but it may also
result in cranial neuropathies (most commonly CN VIII, but also
CN II), spinal stenosis with resulting myelopathy, radiculopathy, or
a combination of these. Serum alkaline phosphatase level is also
elevated in Paget disease.

Question 14

systemic
lupus erythematosus (SLE)

Answer 14

systemic
lupus erythematosus (SLE). This is an autoimmune disorder
characterized by multiorgan involvement and presence of various
antibodies including anti–double-stranded DNA and anti-Smith
antigen. There are specific diagnostic criteria based on
hematologic, dermatologic, neurologic, renal, cardiac, and
serologic features.
SLE may involve both the CNS and the peripheral nervous
system. Neuropsychiatric manifestations of SLE include cognitive
dysfunction, depression, anxiety, and psychosis. Headaches and
seizures are among the most common neurologic manifestations;
others include aseptic meningitis, chorea, and myelopathy. There is an increased risk of
ischemic strokes due to a variety of mechanisms including
cardioembolism, antiphospholipid antibody–associated thrombosis, premature intracranial atherosclerosis, and rarely secondary
cerebral vasculitis. Intracerebral hemorrhage may also occur.
Peripheral nervous system manifestations include cranial
neuropathies, peripheral mononeuropathy or mononeuritis
multiplex, demyelinating or axonal polyneuropathy, and
plexopathy.

Question 15

Systemic sclerosis

Answer 15

Systemic sclerosis is a multiorgan disorder that leads to fibrosis.
Scleroderma is the term used to describe the skin thickening that is
seen in this disorder. Subcutaneous calcinosis, Raynaud
phenomenon, esophageal dysfunction, sclerodactyly, and
telangiectasia (CREST) syndrome is seen in some patients with
systemic sclerosis. The diagnosis is made on the basis of the
presence of clinical features and antibodies against centromeres
and topoisomerases. Intracerebral vasculopathy leading to TIAs,
ischemic stroke, or intracranial hemorrhage may occur. Peripheral
nervous system manifestations include carpal tunnel syndrome,
trigeminal neuropathy, peripheral polyneuropathy, and
mononeuritis multiplex

Question 16

Sjögren syndrome

Answer 16

Sjögren syndrome is an inflammatory multiorgan disorder
primarily affecting exocrine glands (such as the salivary and
lacrimal glands), leading to xerostomia and xerophthalmia (which
when severe can lead to keratoconjunctivitis sicca). Sjögren
Peripheral nervous system involvement in Sjögren syndrome
manifests most commonly as a distal predominantly sensory or
mixed sensorimotor axonal polyneuropathy. A sensory
neuronopathy, or dorsal root ganglionopathy, as depicted in this
case, may occur, and results from involvement of the dorsal root
ganglia. With sensory neuronopathy, the sensory loss may not
follow a length-dependent pattern but rather can affect the face or
trunk before distal segments of the limbs (discussed further in
Chapter 9). Sensory ataxia is often prominent in such cases. Other
manifestations of Sjögren syndrome include isolated small-fiber
neuropathy (without large-fiber involvement), autonomic
neuropathy, and cranial neuropathy. CNS manifestations of Sjögren
syndrome are uncommon but include cognitive dysfunction, focal
brain lesions most often affecting subcortical white matter, aseptic
meningitis, optic neuritis, and myelopathy.
Diagnosis is made on the basis of the presence of symptoms of
xerostomia and xerophthalmia, objective documentation of
xerophthalmia with Schirmer test, serologic testing for the
autoantibodies anti-Ro (SSA) or anti-La (SSB), and/or minor
salivary gland biopsy. Treatment is a combination of symptomatic
therapies and immunosuppressants in some cases.

Question 17

rheumatoid arthritis

Answer 17

Atlanto-axial dislocation is most common in patients with
rheumatoid arthritis, a polyarticular symmetric inflammatory
disorder. In addition to an inflammatory arthritis, other features
include subcutaneous nodules, hypersplenism, amyloidosis,
scleritis, cardiac, and pulmonary involvement. Diagnosis is made
on the basis of the presence of clinical features, rheumatoid factor,
and cyclic citrullinated peptide. Atlanto-axial dislocation in
rheumatoid arthritis results from inflammation and resulting laxity
of the ligaments, with pannus formation. Myelopathy may also
occur. The most common neurologic manifestation of rheumatoid
arthritis is carpal tunnel syndrome. Other neurologic
manifestations of rheumatoid arthritis include headaches,
compressive mononeuropathies, distal sensorimotor
polyneuropathy, mononeuritis multiplex, Brown syndrome
(dysfunction of the superior oblique tendon sheath complex, which
could be congenital or acquired, in which case rheumatoid arthritis
is one of the causes), and rarely ischemic stroke.

Question 18

systemic necrotizing vasculitides

Answer 18

polyarteritis nodosa (PAN), Wegener granulomatosis, Kawasaki disease, and Churg–
Strauss syndrome are systemic necrotizing vasculitides involving
medium and small vessels. These diseases typically involve
multiple organs and often manifest with prominent constitutional
symptoms. Neurologic manifestations of the systemic vasculitides
of medium and small vessels include seizures, mononeuritis
multiplex, cranial neuropathies (with the most frequently involved
being cranial nerve VIII), and peripheral polyneuropathies. The
neuropathy seen in these vasculitides is a necrotizing vasculitic
ischemic neuropathy due to involvement of vasa vasorum. a nerve biopsy specimen demonstrating perivascular
neutrophilic inflammatory infiltrate with necrosis. Arteritis of
cerebral blood vessels may also lead to ischemic stroke.

Question 19

Diagnosis polyarteritis nodosa (PAN), Wegener granulomatosis, Kawasaki disease, and Churg–
Strauss syndrome

Answer 19

polyarteritis nodosa (PAN), Wegener granulomatosis, Kawasaki disease, and Churg–
Strauss syndrome are systemic necrotizing vasculitides involving
medium and small vessels.
Although overlap occurs in these different disorders, certain
features help distinguish them. Diagnostic criteria for Churg–
Strauss syndrome include asthma, eosinophilia, and sinus and
pulmonary involvement. Features of Wegener granulomatosis
include glomerulonephritis, paranasal sinusitis, and pulmonary
involvement. The presence of granulomas on biopsy and the
presence of cytoplasmic antineutrophil cytoplasmic (C-ANCA)
antibody and antibodies to proteinase-3 allow for the diagnosis of
Wegener granulomatosis.
Polyarteritis nodosa leads to a vasculopathy in multiple organ
systems. It presents with prominent constitutional symptoms,
renal, cardiac, and gastrointestinal involvement, and may be
associated with chronic hepatitis B infection. Skin manifestations
include livedo reticularis, skin ulcerations, and subcutaneous
nodules. Abdominal angiogram characteristically demonstrates
small aneurysms in mesenteric arteries.
Kawasaki disease is a disorder of childhood and is characterized
by acute onset of fever, conjunctivitis, mucositis, polymorphous
rash, lymphadenopathy, and other findings, including increased
risk coronary artery aneurysms; neurologic involvement includes
the occurrence of aseptic meningitis

Question 20

Takayasu arteritis (pulseless disease)

Answer 20

Takayasu arteritis, or pulseless disease, a large-vessel vasculitis
most common in females of Asian descent. Commonly involved
vessels include the subclavian arteries, but the aorta and cerebral
vessels can also be involved, leading to ischemic stroke as in the
case depicted in this question. Takayasu arteritis manifests with
constitutional symptoms and symptoms related to organ ischemia
such as peripheral claudication. Treatment is with
immunosuppression and in some cases surgical or endovascular
treatment of vessel stenosis or occlusion.

Question 21

Behçet disease

Answer 21

Behçet disease is a systemic inflammatory disorder that typically
affects multiple organs, including the eyes, skin, gastrointestinal
tract, joints, and vascular system. Uveitis and orogenital ulcers are
characteristic manifestations. Diagnostic criteria include recurrent
oral ulceration, plus two of the following: recurrent genital
ulceration, eye lesions including uveitis, skin lesions (such as
papulopustular lesions), or a positive pathergy skin test. Patients
may also have arthritis, subcutaneous thrombophlebitis, deep
venous thrombosis, and gastrointestinal lesions.
Behçet disease is most common in younger women of
Mediterranean or East-Asian descent. The most common CNS
manifestation is headache. CNS involvement may also include focal
inflammatory brain lesions most commonly affecting the basal
ganglia and/or brain stem. Progressive personality change,
psychiatric disorders, and dementia may develop. Increased
intracranial pressure associated with venous sinus thrombosis is
another potential manifestation of CNS involvement. Unlike other
systemic vasculitides, peripheral nervous system involvement with
Behçet disease is rare, although peripheral neuropathy or
myopathy may occur

Question 22

antiphospholipid antibody syndrome
(APLS)

Answer 22

APLS is a disorder of coagulation resulting from the presence of
circulating antibodies against phospholipid-bound proteins such as
anticardiolipin antibodies and lupus anticoagulant antibodies. In
addition to venous and less commonly arterial thrombosis, other
neurologic manifestations seen in APLS include chorea, headaches,
and seizures.
While several systemic diseases are associated with increased risk
of thrombosis, of those listed, antiphospholipid antibody syndrome
(APLS) is the most likely to cause thrombosis that may involve the
CNS. APLS and most of the so-called hereditary thrombophilias,
including G20210 A prothrombin polymorphism, mutation in the
methylene tetrahydrofolate reductase gene (leading to
hyperhomocysteinemia), factor V Leiden, antithrombin III
deficiency, and protein C and S deficiency, lead to venous
thrombosis. Venous sinus thrombosis is the most common
neurologic manifestation of these disorders, and could lead to
venous infarction. Ischemic infarcts may also occur secondary to
paradoxical emboli to the cerebral vasculature from the venous
system through an intracardiac right-to-left shunt. Arterial
thrombosis may also occur.

Question 23

sarcoidosis

Answer 23

Sarcoidosis is a granulomatous, immune-mediated disorder that
may involve multiple organ systems including (but not limited to)
the lungs (most commonly), skin, heart, and central and peripheral
nervous system. In the United States, it is more common in AfricanAmerican women. Neurologic signs or symptoms as the primary
presentation are rare; less than 10% of sarcoidosis cases present
with extrapulmonary involvement leading to diagnosis. The most
common presentation of neurosarcoidosis is cranial neuropathy,
with cranial nerve VII being the most frequently affected. Multiple
cranial neuropathies may occur in some patients. Other neurologic
manifestations include aseptic meningitis (as in the case presented
in this question), hydrocephalus, parenchymal disease/mass lesion,
myelopathy, small- and large-fiber peripheral neuropathy, and
myopathy. Hypothalamic or pituitary involvement may lead to
endocrinopathy.
The diagnosis of sarcoidosis is established on the basis of the
history, examination, and demonstration of noncaseating
granulomas on biopsy. Serum angiotensin-converting enzyme
(ACE) is neither sensitive nor specific, but increased serum ACE
levels are a marker of disease activity. In patients with known
systemic sarcoidosis, neurosarcoidosis is diagnosed in the setting of
neurologic signs or symptoms and/or findings on CSF or MRI of
the brain or spine (although alternative causes, such as in CNS
infections in sarcoidosis patients being treated with
immunosuppressive therapy must also be considered and
excluded). Diffuse leptomeningeal enhancement, often with
predominance at the base of the brain, is the classic finding,
although focal parenchymal enhancing brain lesions can also occur
( in the splenium of the corpus callosum) as
can intramedullary or extramedullary enhancing spine lesions.

Question 24

Tatalaksana sarcoidosis

Answer 24

Treatment is with immunosuppressive therapy including
corticosteroids and, in some cases, steroid-sparing agents such as
methotrexate. TNF-alpha blocking agents have also been used as
well as other cytotoxic agents.

Question 25

cerebral salt wasting

Answer 25

cerebral salt wasting. This results from excessive renal losses of
sodium and is seen in patients with severe CNS dysfunction. Unlike
patients with syndrome of inappropriate antidiuretic hormone
secretion (SIADH) who are typically euvolemic, in cerebral saltwasting syndrome, the patient is hypovolemic, and the treatment is
with salt supplementation and intravenous isotonic (or sometimes
hypertonic) fluid administration. The pathophysiology of cerebral
salt-wasting syndrome is not clear, but it may in part relate to
increased levels of atrial natriuretic peptide released from the
cardiac atria.

Question 26

syndrome of inappropriate antidiuretic hormone

secretion (SIADH)

Answer 26

SIADH may occur following head trauma, neurosurgery, SAH
and with paraneoplastic ectopic antidiuretic hormone production.
Several medications may also cause SIADH. Treatment of SIADH is
with fluid restriction and correction of underlying causes; in severe
cases, diuretics may be used. Vasopressin receptor antagonists are
being investigated in the neurocritical care setting.

Question 27

postpartum cerebral angiopathy

Answer 27

postpartum cerebral angiopathy, a disorder along the spectrum of
reversible cerebral vasoconstriction syndrome. The
pathophysiology of this disorder is unclear but is related to the
occurrence of multifocal vasospasm. Clinically, patients present
most commonly with headache, although seizure and/or focal
neurologic deficit may occur. This disorder is typically benign,
responsive to calcium channel blockers and/or corticosteroids.
Rarely, ischemic strokes occur. Small cortical subarachnoid
hemorrhages have also been reported.
Normal blood pressure and urine protein level distinguish
postpartum cerebral angiopathy from preeclampsia

Question 28

Venous sinus thrombosis during pregnancy

Answer 28

Venous sinus thrombosis can occur during pregnancy or in the
postpartum period. In addition to headache and other signs and
symptoms of increased intracranial pressure, seizures can occur.
A CT scan with contrast would be of little utility in this case; it
may show a triangular area of central hypodensity surrounded by a
rim of hyperintensity in the superior sagittal sinus (the so-called
empty delta sign), but absence of this sign would not exclude the
diagnosis. Cerebral angiogram is not indicated, although if this
patient’s condition deteriorates significantly, venogram with
venous thrombectomy may be necessary.
Transcranial Doppler ultrasonography could be used to exclude
vasospasm as occurs in postpartum angiopathy.
Pregnancy and the postpartum period are
hypercoagulable states, predisposing to venous sinus thrombosis. In
pregnancy, levels of several of the procoagulant factors are
elevated, including fibrinogen and factors VII, VIII, IX, and X.
These elevations, associated with a reduction in protein S levels,
increase susceptibility to venous thrombosis

Question 29

Gestational hypertension

Answer 29

Gestational hypertension is the presence of hypertension without
associated proteinuria occurring beyond 20 weeks of gestation

Question 30

Eclampsia

Answer 30

Preeclampsia is characterized by gestational hypertension and
proteinuria, often associated with edema in the face and hands.
Eclampsia is the occurrence of seizures in association with
hypertension and edema during pregnancy or in the postpartum
period. The pathophysiology may relate to impaired trophoblast
invasion of the endometrium and immune-mediated and
endocrinologic mechanisms. Associated symptoms may include
headache, visual disturbance, and epigastric abdominal pain.
Postpartum eclampsia is more commonly associated with
complications including disseminated intravascular coagulation and
respiratory distress. In more severe cases, ischemic stroke,
intracerebral hemorrhage, and/or posterior reversible
encephalopathy syndrome may occur.

Question 31

Tatalaksana eclampsia

Answer 31

Management of eclampsia includes delivery (which should be the
priority if the pregnancy is at or close to term) and intravenous
medications such as hydralazine or labetalol for blood pressure
reduction (although excessive reductions should be avoided to
maintain fetal blood flow). Angiotensin-converting enzyme
inhibitors should be avoided given potential effects on the fetal
kidney. Intravenous magnesium sulfate should be administered for
the control and prevention of seizures, and should be used in this
patient. Close monitoring is necessary as magnesium toxicity may
lead to maternal respiratory distress. The use of AEDs is
controversial, but medications that depress the fetus, such as
pentobarbital or phenobarbital, should be avoided; oral diazepam
is likely to be of little utility in seizure control and may depress the
fetus.

Question 32

restless legs
syndrome (RLS) during pregnancy

Answer 32

RLS may first present during pregnancy, and preexisting RLS often worsens during this state. RLS is associated with
iron deficiency, which is not uncommon during pregnancy. Testing
serum ferritin level is indicated, and iron supplementation should
be initiated if the ferritin level is less than 50 ng/mL.