A 39-year-old man presents with a new-onset, asymmetrical
postural tremor. Which of the following is consistent with a
diagnosis of Wilson disease?
a. Elevated urinary copper, elevated serum ceruloplasmin, and
elevated serum copper levels
b. Reduced urinary copper, elevated serum copper level, reduced
serum ceruloplasmin
c. Caudate atrophy on magnetic resonance imaging
d. Elevated aspartate aminotransferase, alanine aminotransfer-
ase, and bilirubin levels
e. Elevated urinary copper level and reduced serum ceruloplasmin
and serum copper
VI.1.
Answer e.
Wilson disease should be considered in patients younger
than 50 years with either hypokinetic or hyperkinetic
movement disorders. Wilson disease can be diagnosed by
identification of Kayser-Fleischer rings on eye examination
and low serum copper and low serum ceruloplasmin with
elevated urinary copper levels. Liver biopsy is sometimes
performed to make the diagnosis.
A 25-year-old woman just received a citalopram prescription
for anxiety. She started taking several over-the-counter medica-
tions. Two days later, the patient had sudden, lighteninglike
movements in her arms and legs, sometimes individually, and
sometimes in her whole body. She seems tremulous as well.
Which of the following steps would be most helpful?
a. Brain magnetic resonance imaging
b. Increase in citalopram because of concerns for functional move-
ment disorder
c. Electroencephalography
d. Assessment of over-the-counter medication ingredients
e. Serum ceruloplasmin test
VI.2. Answer d.
The patient has myoclonus, which may be due to serotonin
syndrome. Citalopram is a selective serotonin reuptake inhib-
itor, and some over-the-counter medications also contain
serotonin. The first step is to assess the over-the-counter med-
ications and discontinue the potentially offending agents.
3 A 35-year-old patient initially has good relief for hemifacial
spasm from onabotulinumtoxinA. However, her symptoms are
worsening. Another management option is which of the follow-
ing steps?
a. Surgical sectioning of the nervous intermedius
b. Microvascular decompression of the facial nerve
c. Stereotactic radiosurgery of the facial nerve
d. Glycerol injection of the facial nerve
e. Stereotactic ultrasound ablation of the facial nerve
VI.3. Answer b.
For patients with hemifacial spasm for whom medical
therapy has failed, microvascular decompression can be
considered but not the other procedures listed here.
4 A patient is asked to stretch out his arms in front of him and
hold his hands up as if stopping traffic. His hands flap forward
repeatedly. This description is an example of which of the
following?
a. Postural tremor
b. Myoclonus (positive)
c. Myoclonus (negative)
d. Chorea
e. Athetosis
VI.4. Answer c.
This is an example of negative myoclonus and may be seen
in selected metabolic disorders.
5 Which of the following is not characteristic of Parkinson
disease?
a. Olfactory dysfunction
b. Length-dependent sensory peripheral neuropathy
c. Rapid eye movement sleep behavior disorder
d. Orthostatic hypotension
e. Mood disorder
VI.5. Answer b.
Peripheral neuropathy is atypical for Parkinson disease.
Common nonmotor characteristics of Parkinson disease
include cognitive dysfunction, dysautonomia, pain, olfac-
tory dysfunction, psychosis, and mood disorders. They
also include several sleep disorders, such as restless leg
syndrome, periodic limb movements of sleep, and rapid
eye movement sleep behavior disorder.
6 for a patient with Parkinson disease who has wearing-off phe-
nomenon while taking levodopa, which of the following adjust-
ments could be considered?
a. Reduce the frequency of levodopa dosing from 3 times daily to
twice daily
b. Change from sustained-release to immediate-release levodopa
c. Ask the patient to take the medication with meals
d. Consider addition of a catechol-O-methyltransferase inhibitor
e. Add amantadine
VI.6. Answer d.
Wearing-off phenomenon is characterized by parkinsonian
symptoms returning before the next dose of levodopa is
typically scheduled. The simplest way to treat this effect is
to increase the dose of levodopa or decrease the time
between doses. Use of the sustained-release formulations
of levodopa medication may also be effective for some
patients. If these strategies prove ineffective, the addition
of a second agent—such as a dopamine agonist, a catechol-
O-methyltransferase inhibitor, or a monoamine oxidase
type B inhibitor—may potentiate the effect of levodopa
and improve the motor fluctuation. Amantadine is typi-
cally used to help dyskinesias.
7 Surgical therapy is indicated to help which characteristic asso-
ciated with Parkinson disease and therapy?
a. Motor fluctuations or dyskinesias, or both, due to medication
b. Medication-refractory freezing of gait
c. Cognitive and emotional changes
d. Postural instability
e. Hallucinations
VI.7. Answer a.
Surgical therapies may be helpful when pharmacologic
treatment proves ineffective or motor fluctuations and dys-
kinesias become disabling. Deep brain stimulation is less
useful for treatment of midline symptoms, such as speech
disturbance and gait. Imbalance or nonmotor characteris-
tics generally do not respond to deep brain stimulation.
8
A patient with Parkinson disease has a gambling habit, which is
unusual for her. Which of the following medications is the most
likely culprit?
a. Amantadine
b. Selegiline
c. Ropinirole
d. Entacapone
e. Trihexyphenidyl
VI.8. Answer c.
Impulse control disorders are a rare adverse effect of dopa-
mine agonists.
9 A 72-year-old woman comes to your clinic for evaluation of a
right-hand tremor. In addition to the tremor, she has had sev-
eral years of intermittent dream reenactment behavior and
almost complete anosmia. On examination, you note diffuse
bradykinesia and hypokinesia. She has a slow, resting tremor of
the right hand and moderate cogwheeling rigidity of all limbs,
which is also worse on the right. Which of the following state-
ments about her treatment is most accurate?
a. Refer the patient for consideration of early subthalamic nucleus
deep brain stimulation
b. Initiate a regimen of high-dose pramipexole
c. Prescribe midodrine for orthostatic hypotension, which often
accompanies her syndrome of symptoms
d. Carbidopa/levodopa should be taken only well before or after
meals
e. Regular exercise should be avoided to reduce fall risk
VI.9. Answer d.
For a patient with Parkinson disease, initiation of dopa-
mine therapy at the lowest effective dose would be recom-
mended before consideration of any type of surgical
intervention. Carbidopa/levodopa is best absorbed when
taken 30 minutes to 1 hour before meals. Regular exercise
is recommended for patients with Parkinson disease.
Orthostatic hypotension would be treated only if present
and symptomatic.
VI.10. A 61-year-old man is seen for imbalance and incoordination
that has lasted 10 months. He has had several episodes of uri-
nary incontinence because he “did not get enough warning.”
He reports total erectile failure. The patient has struck his hus-
band during what appear to be violent dreams. His examina-
tion shows axial rigidity and dysmetria during finger-nose-finger
maneuvers bilaterally. What is the most likely diagnosis?
a. Fahr disease
b. Multiple system atrophy
c. Parkinson disease
d. Pure autonomic failure
e. Wilson disease
VI.10. Answer b.
Rapid eye movement sleep behavior disorder strongly pre-
dicts an underlying synucleinopathy, and the combination
of parkinsonism (rigidity), cerebellar signs (dysmetria), and autonomic dysfunction (incontinence) is characteris-
tic of multiple system atrophy. The other answer choices
are causes of parkinsonism, cerebellar dysfunction, or
autonomic failure, but not all 3.
VI.11. A 68-year-old woman reports progressive gait unsteadiness
over 18 months. She has fallen at least 3 times, always back-
wards. She has given up reading, despite its being a favorite
pastime, because her eyes cannot track the words on the page.
Examination shows a limited downgaze that can be overcome
with doll’s eye maneuver, symmetrical bradykinesia, and retro-
collis. Which of the following histologic findings is most likely?
a. Calcification of basal ganglia
b. Inclusions of α-synuclein in oligodendrocytes
c. Lewy bodies in striatum and cortex
d. Polymorphic double-stranded tau filaments
e. Tau-containing globose neurofibrillary tangles
This patient has progressive supranuclear palsy, which is
characterized histologically by neuronal loss, gliosis, and
flame-shaped and globose neurofibrillary tangles contain-
ing 4-repeat tau.
VI.12. A 70-year-old man with hypertension, hyperlipidemia, and dia-
betes mellitus is evaluated for slowing of gait. He walks with a
shortened stride length and slow pace but normal base. He has
lower limb rigidity and bradykinesia, with essentially normal
upper limb function. Which of the following magnetic reso-
nance imaging findings is most likely?
a. Globus pallidus calcification
b. Left frontal cortex restricted diffusion
c. Midbrain atrophy (hummingbird sign)
d. Bilateral periventricular T2 hyperintensity
e. Pontine atrophy (hot cross bun sign)
Answer d.
This patient has lower-body parkinsonian signs typical of
vascular parkinsonism, made more likely because of his
multiple vascular risk factors. The corresponding ischemic
changes typically are seen in the deep white matter bilater-
ally, rather than cortically or unilaterally.
VI.13. Generalized surface electromyography (EMG) bursts of less than
70 ms and of high amplitude can be seen in which of the fol-
lowing conditions?
a. Spinal cord compression
b. Basal ganglia disease
c. Brainstem encephalitis
d. Infectious or inflammatory encephalitis
e. Brain tumor
Cortical myoclonus, consisting of short-duration jerks, can
be focal, multifocal, or generalized. Surface EMG of corti-
cal myoclonus records bursts lasting less than 70 ms. Focal
cortical myoclonus originates from a hyperexcitable inflam-
matory, neoplastic, or vascular lesion of the sensorimotor
cortex.
VI.14. What is the electrophysiologic hallmark that distinguishes essen-
tial tremor from dystonia tremor?
a. Electromyography (EMG) bursts alternate between agonist and
antagonist muscles in essential tremor and cocontract in dys-
tonic tremor
b. Essential tremor is associated with an abnormal posture
c. Dystonic tremor is more regular and rhythmic
d. There is no way to distinguish between the 2
e. EMG bursts of dystonic tremor have higher amplitude than
essential tremor
14 Answer a.
When a tremor occurs in a limb that also has dystonic
contractions, the tremor is thought to result from phasic
dystonia.
VI.15. Medication-refractory essential tremor can be treated with
which of the following procedures approved by the US Food
and Drug Administration?
a. Magnetic resonance–guided focused ultrasound thalamotomy
b. Gamma knife thalamotomy
c. Focused ultrasound pallidal ablation
d. Surgical pallidal ablation
e. Subthalamic nucleus deep brain stimulation
15 Answer a.
Refractory and disabling essential tremor can respond to
deep brain stimulation of the ventral intermediate nucleus
of the thalamus or to stereotactic thalamotomy. Completed
surgically or with focused ultrasound, thalamotomy is
typically done unilaterally because bilateral thalamotomy
results in dysarthria and other intolerable adverse effects.
VI.16. Which of the following medications is least likely to cause
tremor?
a. Corticosteroids
b. Lithium
c. Amiodarone
d. Albuterol
e. Lisinopril
16 Answer e.
Many medications and drugs may enhance a physiologic
tremor. This topic is detailed in Box 71.1.
VI.17. A 48-year-old woman is referred for “abnormal movements”
that have gradually worsened over the past 3 years. On exami-
nation, you find dancelike movements of all limbs and mild
cognitive impairment. She has a family history of a father with
similar movements and dementia in his 70s. What are you most
likely to find on diagnostic testing?
a. Genetic testing showing 15 and 21 CAG repeats in the HTT genes
b. Normal results on head magnetic resonance imaging (MRI)
c. Three-Hz resting tremor on electrophysiologic testing
d. Throat swab positive for streptococcus
e. Bilateral caudate hypometabolism on positron emission tomog-
raphy
17 Answer e.
The clinical vignette is of chronic progressive chorea with
cognitive involvement. The family history of a father with
a similar disorder is suggestive of Huntington disease.
Positron emission tomography is likely to show bilateral
caudate hypometabolism. Genetic testing in Huntington
disease shows CAG repeats of typically greater than 35.
Head MRI is likely to show caudate and putamen atrophy.
Streptococcus is unrelated to Huntington disease and is
linked to childhood chorea (Sydenham chorea). A resting
tremor is unlikely in Huntington disease.
VI.18. Which of the following statements is correct about primary tor-
sion dystonia (DYT-Tor1A)?
a. DYT-Tor1A typically presents in adulthood
b. DYT-Tor1A is due to a triplet (GAG) deletion in the TOR1A gene
c. DYT-Tor1A frequently leads to cervical dystonia
d. The mutant protein accumulates as cytoplasmic inclusions
e. DYT-Tor1A frequently presents with parkinsonism, tremor, and
myoclonus
18 Answer b.
Primary torsion dystonia is caused by a triplet (GAG) dele-
tion in the TOR1A gene, which encodes for torsinA pro-
tein. DYT-Tor1A typically presents in childhood with limb
onset of dystonia followed by generalization and sparing of
craniocervical regions. TorsinA accumulates in perinu-
clear inclusions.
19 Answer d.
Meige syndrome involves forceful opening or closing of the
jaw, retraction or pursing of the lips, spasm of the platysma,
and, possibly, tongue protrusion. Breathy voice is sugges-
tive of spasmodic dysphonia (abductor type). Unilateral
eyelid closure may be seen in hemifacial spasm. Focal limb
dystonia is not observed in Meige syndrome. Trunk dysto-
nia may be part of a focal or segmental dystonia.
VI.20. A 55-year-old woman presents with a 2-year history of progres-
sively unsteady gait, slurred speech, and handwriting decline.
She reports urinary incontinence and orthostatic lightheaded-
ness. She also has vivid dreams and has kicked and punched
her husband in her sleep on 2 occasions. She drinks 1 glass of
wine nightly. Magnetic resonance imaging (MRI) of the brain
shows subtle cerebellar atrophy. Which of the following is the
most likely diagnosis?
a. Chronic alcohol-related ataxia
b. Multiple system atrophy (MSA)
c. Spinocerebellar ataxia
d. Friedreich ataxia
e. Vitamin E deficiency
Answer b.
The combination of cerebellar ataxia associated with auto-
nomic symptoms and rapid eye movement sleep disorder is
highly suspicious for MSA, cerebellar subtype. The presence
of rapid eye movement disorder is highly associated with
neurodegenerative synucleinopathies, and none of the other
choices fit this category. The brain MRI may show minimal
findings early in MSA and may not show the classic hot
cross bun sign, or pontine atrophy. The patient’s alcohol con-
sumption is unlikely sufficient to cause alcoholic ataxia.
Vitamin E deficiency and Friedreich ataxia are associated
with sensory neuropathies but not with autonomic dysfunc-
tion. Spinocerebellar ataxias are not associated with auto-
nomic failure or rapid eye movement sleep disorder.
VI.21. A 30-year-old man presents with episodes of clumsy gait, dou-
ble vision, and slurred speech that last up to several hours.
These initially occurred once per month but have increased in
frequency to daily. They are often triggered by hot showers,
caffeine or alcohol consumption, or stress. Previously, his con-
dition reverted to normal between attacks, but recently, the
patient feels residual baseline gait clumsiness. Examination
shows mild wide-based gait and slightly slurred speech with
bilateral gaze-evoked nystagmus. Which of the following is the
best strategy to identify the cause of his episodes?
a. Brain magnetic resonance imaging (MRI)
b. Alcohol level during an episode
c. Vitamin B12 level
d. Genetic testing
e. Autonomic testing
21 Answer d.
The clinical history is typical for episodic ataxia type 2,
and the diagnosis is established with genetic testing.
Alcohol intoxication can produce an acute episodic ataxia,
but the other triggers are not consistent with this. Chronic
alcoholic ataxia typically shows gait and lower limb ataxia,
with sparing of upper limbs and eye signs. Brain MRI
structural abnormalities or vitamin B12 deficiency typically
result in a chronic static or progressive ataxia, not episodic
ataxia. Autonomic dysfunction is seen with multiple sys-
tem atrophy, which is also a chronic progressive ataxia.
.
A 60-year-old woman presents with a 2-month history of rap-
idly progressive clumsy speech, unsteady gait, limb incoordina-
tion, vertigo, and nausea. She needs consistent use of a
wheelchair. Clinical examination findings are of a moderately
severe pancerebellar ataxia. Brain magnetic resonance imaging
shows cerebellar atrophy without abnormal enhancement.
Cerebrospinal fluid (CSF) shows a normal cell count but 7 oligo-
clonal bands (upper limit of normal, 4 bands) and is otherwise
negative for bacterial, viral, or fungal tests. The patient believes
her cancer screens are up to date, and she has no known his-
tory of malignancy. Several tests were ordered. Which of the
following is the most likely laboratory abnormality?
a. Serum and CSF paraneoplastic panel
b. Visual evoked responses
c. Genetic testing
d. Vitamin E level
e. Inborn errors of metabolism
22 Answer a.
The clinical scenario is highly suspicious for a paraneo-
plastic cerebellar ataxia, given the rapidly progressive and
disabling course in an otherwise healthy patient. The
increased number of oligoclonal bands in CSF raises suspi-
cion for an inflammatory cause. However, the lack of white
matter abnormalities and focal cerebellar atrophy makes
multiple sclerosis unlikely, and thus, visual evoked
responses will probably be normal. Infectious causes are
unlikely given the lack of astructural infectious lesions (eg,
abscess) and the negative CSF testing. Genetic ataxias are
classically slowly progressive in late life, whereas inborn
errors of metabolism usually manifest in childhood
VI.23. A 16-year-old girl presents with clumsiness and constant falls.
These symptoms have progressively worsened during the past
several months. On physical examination, she has upper- and
lower-extremity limb ataxia, with an absence of patellar and
ankle deep tendon reflexes. The patient has a deficit on posi-
tion and vibration sense, with intact pain and temperature sen-
sation. Kyphoscoliosis is appreciated on examination. Magnetic
resonance imaging of the brain and spine does not show cere-
bellar atrophy but atrophy in the spinal cord and medulla.
Friedreich ataxia is suspected. Which of the following is correct
about Friedreich ataxia?
a. Friedreich ataxia is the most common autosomal dominant
hereditary ataxia
b. It is caused by an unstable expansion of a trinucleotide CAG trip-
let repeat of the frataxin gene
c. Nerve conduction studies have shown reduced or absent com-
pound motor action potentials, consistent with axonal motor
neuropathy, and normal sensory nerve action potentials
d. Cerebellar atrophy is present in Friedreich ataxia
e. The most common cause of death in Friedreich ataxia is cardiac
complications
23 Answer e.
Friedreich ataxia is the most common autosomal recessive
hereditary ataxia, caused by an unstable expansion of a tri-
nucleotide GAA triplet repeat of the frataxin gene. Nerve
conduction studies have shown reduced or absent sensory
nerve action potentials consistent with sensory neuropa-
thy and normal compound motor action potentials. There
is no cerebellar atrophy, but atrophy of the spinal cord is
present.
VI.24. Ataxia disorders associated with DNA repair defects include all
of the following except which characteristic?
a. Xeroderma pigmentosum
b. Refsum disease
c. Ataxia-telangiectasia–like disorder
d. Cockayne syndrome
e. Ataxia with oculomotor apraxia type 2
24 Answer b.
Refsum disease is due to an inborn error of lipid metabo-
lism. Deficiency in the peroxisomal enzyme of PHYH or
PEX7 leads to phytanic acid accumulation and neurotoxic-
ity. This results in early pigmentary retinal degeneration
and night blindness, variably accompanied by peripheral
neuropathy, deafness, anosmia, ataxia, ichthyosis, and car-
diac arrhythmias. Treatment is dietary reduction of phy-
tanic acid and plasmapheresis for severe symptoms. The
other disorders encompass DNA repair defects. Xeroderma
pigmentosum is caused by DNA excision repair defects
reported in at least 8 different associated genes. Ataxia-
telangiectasia–like disorder results from homozygous
mutations encoding MRE11 protein, a double-stranded
DNA repair enzyme. Cockayne syndrome is caused by a
mutation in excision repair cross-complementing protein.
Ataxia with oculomotor apraxia type 2 is caused by sena-
taxin gene (SETX) mutations, which probably affect DNA
and RNA helicase repair.
VI.25. A 35-year-old man presents with a 2-year history of slowly pro-
gressive gait unsteadiness and slurred speech. His older sister
and paternal aunt had similar symptoms starting at about the
same age. His father has a diagnosis of Parkinson disease. The
patient’s examination shows bulging eyes, ataxic speech,
upper- and lower-limb ataxia, wide-based ataxic gait, absent
lower-limb reflexes, and distal lower-limb atrophy. The most
likely diagnosis is which of the following?
a. Spinocerebellar ataxia (SCA) type 3
b. SCA type 2
c. SCA type 6
d. Dentatorubral-pallidoluysian atrophy
e. Biallelic AAGGG expansion in the RFC1 gene
VI.25. Answer a.
SCA type 3 is the most common autosomal dominant ataxia,
and its typical onset is in young adulthood. In addition to
cerebellar ataxia, phenotypes include levodopa-responsive
parkinsonism that can resemble Parkinson disease, dystonia,
amyotrophy, or neuropathy. Eye abnormalities are com-
monly reported, including bulging eyes and ophthalmople-
gia. SCA type 2 can also occur in young adulthood, with
parkinsonism phenotype and eye signs of slow saccades.
SCA type 6 typically occurs in late adulthood and is a pure
cerebellar ataxia with downbeat nystagmus. Dentatorubral-
pallidoluysian atrophy with onset after age 20 years may
include ataxia, dementia, choreoathetosis, and psychiatric
characteristics. Biallelic AAGGG expansion in RFC1 is the
most common cause of late-onset recessive ataxia.
VI.26. Which of the following statements is true regarding Sydenham
chorea?
a. Sydenham chorea is common in children younger than 3 years
b. Its cause is typically Staphylococcus aureus
c. Chorea typically persists into adulthood
d. Personality changes may occur along with the motor manifesta-
tions of chorea
e. Treatment should include azithromycin and corticosteroids
VI.26. Answer d.
Sydenham chorea is considered a manifestation of rheu-
matic fever, a sequela of group A β-hemolytic streptococcal
infection. It typically occurs between the ages of 5 and 15
years, and the chorea often improves. Personality changes
may occur near the onset of motor dysfunction, with symp-
toms of inattention, anxiety, emotional lability, and obses-
sive compulsiveness. For all children with Sydenham
chorea, treatment includes secondary prevention with
daily oral penicillin or monthly intramuscular penicillin
injections until age 21 years.
VI.27. A 7-year-old girl presents with gradual, progressive dystonia of
her right lower extremity. She has no cognitive issues or sei-
zures. Eye examination has normal results. Magnetic resonance
imaging of the brain is normal. The girl’s maternal grand-
mother had cerebral palsy. Which one of the following treat-
a. OnabotulinumtoxinA
b. Levodopa/carbidopa
c. Clonazepam
d. Gabapentin
e. Baclofen
VI.27. Answer b.
Dopa-responsive dystonia (DYT5) is an autosomal domi-
nant condition that presents before age 10 years with pro-
gressive dystonia and a sustained dramatic response to low
doses of levodopa. Girls are preferentially affected over
boys (≥2:1). Patients often present with a gait disturbance
from dystonia of the lower extremity. As the disorder pro-
gresses, dystonia becomes more generalized. An empirical
trial of levodopa should be considered for any child with
VI.28. An infant child has gradual, progressive visual disturbance,
hearing loss, and ataxia. Eye examination shows retinitis pig-
mentosa. Neurologic examination shows bilateral hearing loss,
peripheral neuropathy, and ataxia. An important test that
might help make the diagnosis is which of the following?
a. Serum phytanic acid
b. Urine organic acids
c. Serum ceruloplasmin
d. Serum vitamin E
e. Blood smear
VI.28. Answer a.
Infantile Refsum disease is an autosomal recessive condi-
tion due to a peroxisomal disorder that results in the
abnormal buildup of a type of fatty acid called phytanic
acid. Common signs of this condition include hearing loss,
retinitis pigmentosa, and peripheral neuropathy.
VI.29. Which of the following is true about juvenile Huntington disease?
a. Patients generally have fewer than 20 trinucleotide (CAG)
expansions
b. Among cases of juvenile-onset Huntington disease, 80% is inher-
ited from an affected father
c. Chorea is often the first sign of the disease
d. Juvenile-onset disease progresses more slowly than adult-onset
disease
e. Juvenile-onset disease has autosomal recessive inheritance
VI.29. Answer b.
Unlike the adult-onset form, 80% of juvenile-onset Huntington
disease is inherited from an affected father. Juvenile-onset
Huntington disease typically has more than 80 CAG repeats.
In contrast to adult patients who present with cognitive
decline, chorea, or psychiatric disease, patients with juve-
nile-onset Huntington disease most often present with par-
kinsonism, speech deficits, intellectual abnormalities, and
seizures. Adolescents with Huntington disease may present
initially with psychiatric illness, followed by chorea or dys-
tonia. The juvenile-onset disease progresses about twice as
rapidly as the adult-onset version.
Last changed14 days ago