Fungsi Luhur Flashcards
Neuro behaviour, Cognitive, demensia
1
Q
Pemeriksaan rutin pada pasien demensia berdasarkan American Academy of Neurology (AAN)
A
vitamin B12,
- darah lengkap, elektrolit, Glukosa, Ur/CT, fungsi liver, thyroid
- depression screening
2
Q
Gejala awal Alzheimer
A
Recent memory impairment
3
Q
Afasia sensorik, letak kelainan di
A
Afasia sensorik karena lesi Di area Wernicke Di lobus temporal superior
4
Q
Mild cognitive impairment, klasifikasi
A
Gangguan kognitif yg tidak mempengaruhi Aktivitas sehari hari. Kognitif umum Masih baik. Gangguan terdapat pada atensi, memory, Bahasa, eksekutif, Atau visuospasial diklasifikasikan sebagai :
- amnestic MCI (memori primer) - nonamnestic MCI ( domain kognitif selain memory, misal bahasa) - multiple domain MCI (lebih Dari satu domain terkena)
5
Q
Alzheimer Disease inheriter
A
Jarang (<5% dari kasus AD)
: autosomal dominan, Dan umumnya muncul sebelum usia 65.
Presenilin-2, presenilin 1 (70-80% early onset aggressive familial AD)
Apolipoprotein A4, variant TREM2 meningkat kan resiko AD
6
Q
Sirkuit papez
A
The circuit of Papez is:
entorhinal cortex → hippocampus → fornix → mammillary bodies
→ anterior nucleus of thalamus → cingulate gyrus → entorhinal
cortex → hippocampus.
7
Q
Macam bentuk memori
A
immediate memory : forward digit span
• - working memory : backwards digit span
• - recent memory : recall Dalam menit/jam. Disimpan pada area hipocampus/parahipocampus. Merupakan yg pertama terserang pada Alzheimer.
• - remote memory : memory jangka panjang
8
Q
FDG pet scan pada Alzheimer Disease
A
FDG-PET scan shows bilateral parietotemporal
hypometabolism,
9
Q
FDG pet scan pada Lewy
body disease
A
Lewy
body disease pada FDG pet scan menunjukkan occipital regions in diffuse
10
Q
Klinis Dementia lewy bodies
A
Trias DLB : Parkinsonism, fluctuating cognitive impairment, and visual
hallucinations
other clinical features may include
dysautonomia, REM sleep behavior disorder, and neuroleptic
sensitivity
11
Q
Tatalaksana Dementia lewy bodies
A
Acetylcholinesterase
inhibitors may be of benefit. Levodopa may worsen hallucinations
and high doses should be avoided in DLB. Neuroleptics have been
associated with increased risk of mortality when used in older
adults with dementia, but in some cases, putative benefits
outweigh risks of use. Typical neuroleptics are generally avoided
due to significant sensitivity, with reactions such as neuroleptic
malignant syndrome, worsening parkinsonism, confusion, or
autonomic dysfunction. If absolutely necessary, especially for
agitated psychotic symptoms, atypical neuroleptics should be tried
cautiously in low doses
12
Q
Pick’s disease
A
Pick’s disease is manifested predominantly by frontal lobe
symptoms such as personality changes, behavioral problems,
apathy, abulia, and poor judgment.
pathologically by
the presence of silver-staining, spherical aggregations of tau
protein in neurons (Pick bodies).
13
Q
Kluver–Bucy type
syndrome
A
caused by
lesions to bilateral anterior temporal lobes/amygdala and is
characterized by hyperorality (tendency to explore objects with
mouth), hypermetamorphosis (preoccupied with minute
environmental stimuli), blunted emotional affect, hypersexuality,
and visual agnosia
14
Q
Frontotemporal Dementia
A
Cognitive
decline does occur, but memory impairment is not the most
prominent feature, distinguishing the frontotemporal dementias
(FTDs) from Alzheimer’s disease. FTD dementia is a general term
for pathologies affecting frontal lobes, included among them is
Pick body pathology.
- onset rata rata 55-60 tahun
15
Q
Gejala lesi orbitofrontal
A
Symptoms of orbitofrontal lesions may include traits of obsessive
compulsive disorder (OCD), disinhibition, hypersexuality, anxiety,
depression, impulsiveness, and antisocial behavior
16
Q
Gejala lesi lobus parietal
A
- Lobus dominan : visuospatial and sensory symptoms
* nondominant: contralateral neglect syndrome.
17
Q
familial frontotemporal dementia (FTD) terkait kromosom
A
Pada familial frontotemporal dementia (FTD), paling banyak berhubungan dengan chromosome 17q21, meskipun chromosomes 3 Dan 9 juga berimplikasi pada kelainan herediter autosomal dominant pada Penyakit ini.
18
Q
Tiga Varian utama FTD /Frontotemporal Dementia
A
There are three major distinct clinical phenotypes of FTD.
- Behavioral variant FTD
- progressive nonfluent aphasia
- semantic dementia, also called
progressive fluent aphasia, or the temporal variant of FTD ; transcortical sensory afasia.
The
behavioral variant FTD is the most common phenotype and
symptoms include personality change, abulia, apathy, social
withdrawal, social disinhibition, impulsivity, lack of insight, poor
personal hygiene, stereotyped or ritual behaviors, hyperphagia,
suddenly new artistic abilities or hobbies, emotional blunting, loss
of empathy, mental rigidity, distractibility, impersistence,
perseverative behavior, impaired organizational and executive
skills
The second phenotype, progressive nonfluent aphasia, is
characterized in early stages by anomia, word-finding difficulty,
impaired object naming, and effortful speech with preserved
comprehension. Spontaneous speech becomes increasingly
dysfluent and speech errors become frequent. Behavior and social interaction remain unaffected until late in the disease at which
point the patient becomes globally aphasic.
The third phenotype is semantic dementia, also called
progressive fluent aphasia, or the temporal variant of FTD. It is
characterized by a progressive speech disturbance with normal
fluency, but impaired comprehension, anomia, and semantic
paraphasias. It may clinically resemble a transcortical sensory
aphasia. There is typically a predominance of left temporal
dysfunction, and/or in face and object recognition, reflecting right
temporal dysfunction
19
Q
Afasia Wernicke terjadi pada lesi topis
A
Lobus temporal dominant
20
Q
Amnesia nonverbal Dan visuospasial terjadi pada lesi
A
Lobus temporal nondominan
21
Q
Disfungsi lobus frontal dapat terjadi pada oklusi
A
Arteri Cerebral Anterior
22
Q
Psychogenic amnesia
A
Psychogenic amnesia has the characteristic finding of loss of
autobiographical memory, sometimes with preserved ability for
new learning.
23
Q
Wernicke’s encephalopathy
A
Wernicke’s encephalopathy, which results from
deficiency in thiamine (vitamin B1), as occurs in malnourishment
such as in alcoholism, is defined by the triad of confusion, ataxia,
and ophthalmoplegia.
24
Q
Gerstmann’s syndrome
A
Gerstmann’s syndrome, which is
characterized by the tetrad of finger agnosia (inability to identify
fingers bilaterally), right–left confusion, dyscalculia (inability to
carry out calculations), and dysgraphia (inability to write). It
localizes to the dominant inferior parietal lobule, particularly the
dominant angular gyrus. A common cause is infarction of the
inferior division of the middle cerebral artery, in which case there
may be associated contralateral visual field deficits. Features may
occur individually
25
anosognosia
a lack
of awareness of an acquired neurologic deficit
26
hemispatial
neglect syndrome, topis lesi
hemispatial
neglect syndrome, consistent with a lesion in the nondominant
hemisphere involving the primary somatosensory cortex (area SI).
A lesion in the thalamus can also lead to a neglect syndrome
27
Dejerine–
Roussy syndrome, or thalamic pain syndrome
Lesi posterolateral thalamus : diawali contralateral hemianesthesia followed
weeks later by pain, hyperesthesia, and allodynia. A similar
delayed central pain syndrome can occur with a lesion to the
medial lemniscus, dorsal columns, or with lesions to the parietal
operculum (the latter is also termed pseudothalamic syndrome).
The spinothalamic tract projects to the ventral posterolateral
nucleus of the thalamus, which in turn projects to the secondary
somatosensory cortex (area SII). A lesion to the primary
somatosensory cortex (area SI) would lead to contralateral loss of
sensation to touch, joint position sense, and vibration, but would
spare pain and temperature sensation, and would not cause a
delayed pain syndrome.
28
Corticobasal syndrome
corticobasal syndrome (CBS), in which alien
limb syndrome occurs. The phenomenon of alien limb is marked by
movement of a limb, sometimes seemingly purposefully, but not
under voluntary control. Alien limb syndrome also occurs with
lesions to the contralateral anterior cerebral artery territory,
involving the corpus callosum or supplementary motor area. Other
features of CBS include parkinsonism, apraxia, and cortical sensory
loss. There are several causes to CBS, including corticobasal
ganglionic degeneration, and progressive supranuclear palsy
29
Biomarkers Alzheimer Disease
* Hippocampal atrophy
* CSF :reduced CSF beta-amyoid1–42 and increased total and phosphorylated CSF tau.
* PET scan : FDGPET hypometabolism temporoparietal bilateral
* White matter changes are common in AD but are not a specific biomarker
30
Fase Alzheimer Disease
Terdiri atas 3 fase :
1. preclinical (where there are no clinical symptoms but there are biomarker changes such as amyloid deposition seen on amyloid imaging),
2. prodromal (where patients have biomarkers positive and early symptoms but not affecting function),
3. Alzheimer’s dementia (where patients have biomarkers and express functional deficits).
31
Struktur otak terkait kesadaran
Consciousness is maintained by a variety of structures, including
the reticular activating system in the brainstem, the thalamus
(particularly the intralaminar nuclei), and the frontal lobes
32
Declarative/explicit memory
Declarative, or explicit memory, involves memory for facts or
experiences. Declarative memory includes semantic knowledge, or
knowledge for facts and objectives, and episodic knowledge, or
knowledge of events. Nondeclarative, or implicit memory, involves
memory of skills and other acquired behaviors, such as ability to
drive a car or ride a bicycle. Lesions to the bilateral medial
temporal lobes leads to loss of predominantly declarative (explicit)
memory, leading to an anterograde amnesia with a retrograde
amnesia involving a specific period prior to injury, but usually with
preservation of more remotely formed memories
33
Capgras’ syndrome
Capgras’ syndrome, which is characterized by
the delusional belief that a person, often a member of the patient’s
immediate family, is an identical-looking imposter
34
Fregoli’s
syndrome
Fregoli’s
syndrome (in which the patient believes that the same person
exists in several disguises
35
intermetamorphosis
intermetamorphosis (the belief that
individuals have swapped identities with each other while
maintaining the same external appearance
36
reduplicative
paramnesia
reduplicative
paramnesia (which overlaps significantly with Capgras’, but there
is a delusion that there are identical places/objects rather than just
people
37
Cotard’s delusion
Cotard’s delusion (a person’s belief that they are dead
or dying
38
delusional misidentification disorders, macam
- capgras
- cotard
- intermetamorphosis
- reduplicative paramnesia
- fregoli
39
Pseudocyesis
Pseudocyesis is not classified under the delusional
misidentification disorders but is a delusion that a person is
pregnant when they are in fact not; the patient may manifest the
signs and symptoms of pregnancy. It is more common in females
but has been reported in males
40
Charles Bonnet syndrome
Charles Bonnet syndrome, a form of release hallucination, is a
condition marked by vivid hallucinations that occur in people with
severe visual impairment due to a variety of reasons, most
commonly ophthalmologic. Patients acknowledge that these
images are hallucinations. This may be mistaken as a delusional
disorder or psychosis, but the patient’s insight into the fact that
these are hallucinations helps rule this out
41
Anton’s syndrome /Anton–Babinski syndrome
Anton’s syndrome, also known as Anton–Babinski syndrome or
visual anosognosia, manifests as cortical blindness with denial of
visual loss and confabulation. This syndrome results from bilateral
lesions of the medial occipital lobes (primary visual and visual
association cortices). A delusional disorder is not suspected, this is
due to a structural cause
42
Balint's Syndrome
Balint’s syndrome ( Balint–Holmes
syndrome), lesi di parieto-occipital.
Trias :optic ataxia (a deficit of
reaching for objects under visual guidance), oculomotor apraxia
(gaze apraxia, inability to voluntarily move the eyes to a new point
of visual fixation despite normal extraocular muscle function), simultanagnosia (inability to visually perceive more than one
object at a time).
This syndrome has been described with a variety
of pathologies including neurodegenerative disorders, progressive
multifocal leukoencephalopathy, bilateral watershed infarcts, and malignancy.
In general, though there are exceptions, lesions of the dorsal
visual pathways that pass through the parieto-occipital regions can
be thought of as leading to an abnormality in detecting “where”:
where an object is in space, how to reach that object while looking
at it. Lesions of the ventral, temporo-occipital pathways lead to an
abnormality of detecting “what”: what an object is
43
human prion diseases; macam
human prion diseases are kuru, CJD, variant
Creutzfeldt–Jakob disease (vCJD) (“mad cow disease”),
Gerstmann–Straüssler–Scheinker syndrome (GSS), and fatal familial
insomnia (FFI)
44
normal pressure
hydrocephalus (NPH)
trias (NPH): cognitive dysfunction, gait impairment
( “magnetic gait”), urinary incontinence.
MRI
: ventriculomegaly, which is out of proportion to cortical
atrophy, transependymal edema.
Terapi : LP (30 to 50 cc) with subsequent
improvement in symptoms predicts a better chance of
improvement from a shunting procedure. Therefore, the first step
in the treatment of this patient should be a lumbar puncture,
possibly followed by shunt procedure (depending on the response
to the fluid evacuation with the lumbar puncture). Patients with
dementia for more than 2 years are less likely to improve with
shunting
45
Gangguan memori pada depresi
Major depression results in poor attention and, subsequently,
immediate recall is often impaired, while short-term memory is
typically preserved
46
Gangguan memori pada Early Alzheimer’s dementia dan Korsakoff’s
disease
Early Alzheimer’s dementia and Korsakoff’s
| disease preserve immediate recall and show impaired learning and
recall of new information
47
Gangguan memori pada transient global amnesia
Pada transient global amnesia (TGA), recent (short term) memory terganggu. Immediate memory,. Remote and procedural memory and
personal identity are retained. typically lasts 12- 24 hours and usually resolves
without deficit. Klinis : bertanya berulang ulang
pathophysiology of TGA is thought to result from functional alterations in the
bilateral medial temporal lobes. It has been associated with
migraine, hypertension, medical procedures, and stressful events,
among others. It Clinically the patients may ask the same questions
over and over each time the examiners come into the room. They
often forget meeting the examiner if the examiner leaves the room
briefly and then returns.
48
human prion diseases, macam
1. kuru,
2. CJD,
3. variant
Creutzfeldt–Jakob disease (vCJD) (“mad cow disease”),
4. Gerstmann–Straüssler–Scheinker syndrome (GSS),
5. fatal familial
insomnia (FFI).
These diseases share the neuropathologic features
of neuronal loss, glial cell proliferation, absent inflammatory
response, and vacuolization of the neuropil, which produces the
characteristic spongiform appearance
49
Creutzfeldt–Jakob disease
CJD is a rapidly progressive dementia
associated with variable extrapyramidal/pyramidal tract signs,
myoclonus, and ataxia, and death typically ensues within 1 year.
Sporadic cases account for 85% to 95%, while 5% to 15% are
familial, with an autosomal dominant pattern of inheritance. The
pathology occurs when the normal prion protein (PrP), which is
primarily an α-helical structure, converts into an abnormal form
containing a higher percentage of β-pleated sheets. The abnormal
form is insoluble, polymerizes, and accumulates intracellularly and
is resistant to proteolysis. The prion protein gene (PRNP) coding
for PrP is located on chromosome 20p
Neuroimaging of CJD includes cortical ribbon sign (restricted
diffusion in the cortex), and increased T2 signal in the caudate,
putamen, and pulvinar of the thalamus
50
Gambaran histopathology Alzheimer Disease
Alzheimer’s disease (AD). It shows amyloid (neuritic) plaques,
which are extracellular collections of amyloid protein deposited on
dendrites and axons. They are composed of β-amyloid proteins.
Amyloid plaques are a characteristic finding in AD. The other
histopathologic findings in AD include intraneuronal neurofibrillary
tangles (paired helical filaments made up of abnormally
hyperphosphorylated tau protein), granulovacuolar degeneration
(neuronal intracytoplasmic granule containing vacuoles), amyloid
angiopathy (amyloid deposition in walls of small and medium sized
arteries), and Hirano bodies (cytoplasmic inclusions composed
mainly of actin and actin-associated proteins)
51
Mekanisme aksi memantine
Memantine is a low-to-moderate
affinity noncompetitive NMDA receptor antagonist and is approved
for moderate–severe dementia in Alzheimer’s disease (AD)
52
Tatalaksana farmakologi Alzheimer Disease
Patients with AD have reduced cerebral production of choline
acetyl transferase, which leads to a decrease in acetylcholine
synthesis and impaired cortical cholinergic function. Donepezil,
rivastigmine, galantamine, and memantine are all medications used
in the treatment of dementia, most commonly AD. Donepezil is a
pure acetylcholinesterase inhibitor. Rivastigmine is a combined
acetylcholinesterase and butyrylcholinesterase antagonist, both of
which result in limiting the breakdown of acetylcholine.
Galantamine is a combined acetylcholinesterase inhibitor and
allosteric nicotinic modulator. Memantine is an NMDA receptor
antagonist that inhibits glutamate stimulation and thus
theoretically limits overactivation and toxicity to remaining
cholinergic neurons. Memantine also has some antagonistic action
at the 5HT3 serotonin receptor
53
Akinetik mutism
Bilateral globus pallidus interna lesions can cause akinetic mutism.
In akinetic mutism, the patient generally has preserved awareness
with open eyes, but remains immobile, mute, and does not respond
to commands. The globus pallidus interna is part of the anterior
cingulate–frontal–subcortical circuit. Recall that bilateral ACA
infarcts to the frontal lobes and other lesions to the medial frontal
lobes are other causes of akinetic mutism.
54
Agnosia
Agnosia is loss of ability to recognize previously known stimuli,
while the specific sense to detect the stimuli is not impaired
55
Prosopagnosia, letak lesi
Prosopagnosia is the inability to recognize faces. Ability to
recognize people using other cues is often preserved. Face
recognition is thought to be a function of the right hemisphere, but
prosopagnosia most commonly occurs with bilateral lesions of thtemporo-occipital regions (bilateral fusiform gyri), as occurs with
bilateral posterior cerebral artery infarction. It can also be seen as
part of more diffuse processes that preferentially affect the
temporal lobes, such as Alzheimer’s disease
56
Topographagnosia
Topographagnosia, a defect in spatial orientation, is marked by
inability to navigate in familiar places, read maps, draw floor maps
of familiar places, and perform similar functions. It localizes to the
nondominant posterior parahippocampal region, infracalcarine
cortex, or nondominant parietal lobe
57
Asomatognosia, topis
Asomatognosia is marked by an indifferent inability to recognize
one’s own body part. It most often localizes to the contralateral
(usually nondominant) superior parietal lobule, the supramarginal
gyrus, and/or its connections. In somatoparaphrenia, a form of
asomatognosia, the patient denies ownership of a limb or limbs and
claims the limb is missing, or has been stolen
58
Misoplegia
Misoplegia is severe hatred of a limb, a rare form of agnosia
seen in hemiparetic or hemiplegic patients following stroke. The
patient may attempt to cut off the limb or otherwise damage it
59
alexia without agraphia, / pure word blindness
alexia without agraphia, or
pure word blindness. Alexia is a loss of reading comprehension
despite normal visual acuity. Ability to read individual letters of a
word is often retained. Writing and language comprehension are
normal in alexia without agraphia. It is a disconnection syndrome,
due to lesions in the dominant (usually left) posterior cerebral
artery territory, commonly involving the medial and inferior
occipitotemporal region and splenium of the corpus callosum. The
patient has a contralateral (usually right) homonymous
hemianopia. While the ipsilateral visual field is intact, words that
are seen cannot be effectively read, as the lesion in the splenium of
the corpus callosum prevents them from being transmitted to
Broca’s area
60
Pure word deafness, or verbal auditory agnosia
Pure word deafness, or verbal auditory agnosia, is marked by
impaired auditory comprehension of language, though hearing per
se (of tones and other nonverbal sounds) is intact; audiogram is
normal in these patients. There is normal comprehension of written
language, distinguishing it from Wernicke’s (sensory) aphasia;
Wernicke’s aphasia is characterized by inability to comprehend,
read, or repeat, with fluent, nonsensical speech. The lesion causing
pure word deafness is most often in the bilateral middle portion of
the superior temporal gyri, sparing Wernicke’s area, but disrupting
its connections with the primary auditory cortex (Heschl’s gyrus)
and temporal lobe association cortices. Cases have been reported
with unilateral dominant hemisphere temporal lobe lesions. This
may be associated with amusia, or agnosia for music.
61
Anomia
Anomia is inability to name objects with otherwise relative
preservation of language expression and comprehension. Patients
are able to recognize the objects but cannot name them. Anomia
usually occurs in association with other features of Broca’s
(expressive) aphasia , though it may occur in
isolation, particularly during recovery of a Broca’s (expressive)
aphasia. Anomia may occur with a variety of lesions, including
dominant hemisphere posterior inferior frontal gyrus and temporal
lesions. It has also been reported to occur in angular gyrus
syndrome, due to lesions of the dominant angular gyrus, in
association with gertsmann syndrome
and constructional difficulties.
62
pseudobulbar affect
pseudobulbar affect,
also known as involuntary emotional expression disorder. The
pathophysiology of pseudobulbar affect is complex, but it most
often occurs in patients with bilateral lesions that disconnect the
corticobulbar tracts from the brainstem cranial nerve nuclei. It is
commonly seen in patients with diffuse subcortical dysfunction, as
occurs with amyotrophic lateral sclerosis, multiple sclerosis, and
following traumatic brain injury but has also been reported in
patients with focal mass lesions or acute infarctions. A
dextromethorphan–quinidine combination has been shown to
reduce and sometimes even eliminate pseudobulbar affect in
patients with a variety of neurologic disorders
63
Amelodia or affective motor aprosodia
Amelodia or affective motor aprosodia localizes to the
nondominant posterior inferior frontal gyrus, the nondominant
hemisphere’s analog to Broca’s area. Similarly, the inability to perceive and understand the emotional content of others’ speech
64
sensory or receptive aprosodia
sensory or receptive aprosodia, localizes to the nondominant
posterior superior temporal gyrus, the nondominant hemisphere’s
analog to Wernicke’s area
65
conduction aphasia, klinis Dan topis
The internal arcuate fasciculus connects Wernicke’s area in the
superior temporal gyrus to Broca’s area in the inferior frontal
gyrus. Lesions in this fasciculus lead to conduction aphasia, in
which repetition is impaired but other aspects of language are
intact
66
transcortical afasia
Transcortical sensory aphasia can be thought of as a Wernicke’s
(receptive) / Broca aphasia but with intact repetition. Transcortical sensory
aphasia may be seen in dominant hemisphere MCA–PCA territory
watershed infarction, thalamic lesions (thalamic aphasia), and in
neurodegenerative disorders such as Alzheimer’s disease.
Transcortical aphasias are also seen in the stages of recovery from
other aphasia syndromes
. This aphasic syndrome is seen with a variety of cortical
and subcortical dominant hemisphere lesions in the frontal lobe,
but is most commonly seen in two general settings. The first occurs
in the setting of watershed infarcts in the dominant hemisphere
ACA–MCA watershed territory, sparing connections between
Wernicke’s and Broca’s area, but impairing speech output due to
disruption of connections between Broca’s area and the
supplementary motor area. The supplementary motor area is
located in the medial aspect of the superior frontal gyrus and can
be thought of as the pacemaker for speech output
67
Foix–Chavany–Marie syndrome
Foix–Chavany–Marie syndrome, also known as anterior opercular
syndrome, is characterized by severe dysarthria, bilateral voluntary
paralysis of the lower cranial nerves with preserved involuntary
and emotional innervation. This syndrome is associated with
bilateral anterior opercular lesions, frequently in the setting of
multiple infarct
68
Aphemia, or pure word mutism
Aphemia, or pure word mutism, also referred to as verbal apraxia,
is marked by an inability to speak fluently, impaired repetition,
and intact auditory comprehension. A pure Broca’s (expressive)
aphasia is characterized by inability to speak, write, name, or
repeat, but intact comprehension. In aphemia, there is retained
ability to write and comprehend written language. The lesion is in
the dominant frontal operculum, anterior and superior to Broca’s
area (posterior inferior frontal gyrus).
69
Pure word deafness, or verbal auditory agnosia
Pure word deafness, or verbal auditory agnosia, is marked by
impaired auditory comprehension of language, though hearing per
se (of tones and other nonverbal sounds) is intact; audiogram is
normal in these patients. There is normal comprehension of written
language, distinguishing it from Wernicke’s (sensory) aphasia;
Wernicke’s aphasia is characterized by inability to comprehend,
read, or repeat, with fluent, nonsensical speech. The lesion causing pure word deafness is most often in the bilateral middle portion of
the superior temporal gyri, sparing Wernicke’s area, but disrupting
its connections with the primary auditory cortex (Heschl’s gyrus)
and temporal lobe association cortices. Cases have been reported
with unilateral dominant hemisphere temporal lobe lesions. This
may be associated with amusia, or agnosia for music.
In nonverbal auditory agnosia, there is agnosia to sounds, such
as the sounds animals make or environmental sounds. This most
often occurs with bilateral anterior temporal lesions, though
nondominant temporal lobe lesions can lead to this as well.
70
Anomia
Anomia is inability to name objects with otherwise relative
preservation of language expression and comprehension. Patients
are able to recognize the objects but cannot name them. Anomia
usually occurs in association with other features of Broca’s
(expressive) aphasia, though it may occur in
isolation, particularly during recovery of a Broca’s (expressive)
aphasia. Anomia may occur with a variety of lesions, including
dominant hemisphere posterior inferior frontal gyrus and temporal
lesions. It has also been reported to occur in angular gyrus
syndrome, due to lesions of the dominant angular gyrus, in
association with Gertsmann’s syndrome
71
syndrome of alexia without agraphia, or
| pure word blindness
syndrome of alexia without agraphia, or
pure word blindness. Alexia is a loss of reading comprehension
despite normal visual acuity. Ability to read individual letters of a
word is often retained. Writing and language comprehension are
normal in alexia without agraphia. It is a disconnection syndrome,
due to lesions in the dominant (usually left) posterior cerebral
artery territory, commonly involving the medial and inferior
occipitotemporal region and splenium of the corpus callosum. The
patient has a contralateral (usually right) homonymous
hemianopia. While the ipsilateral visual field is intact, words that
are seen cannot be effectively read, as the lesion in the splenium of
the corpus callosum prevents them from being transmitted to
Broca’s area.
72
Apraxia, macam
Apraxia is characterized by an impaired ability to execute a
previously known task, in the absence of motor weakness,
incoordination, or a deficit in comprehension.
Macam :
1. Ideomotor apraxia
2. Conductional apraxia
3. Ideational apraxia
4. Conceptual apraxia
5. Disassociation apraxia
73
Ideomotor apraxia, klinis Dan topis
ideomotor apraxia, which is suggested by use of a body part as an
object during pantomime, as well as the unusual movements and
postures. Patients with ideomotor apraxia understand the
movement that they are supposed to execute, and achieve the
general, overall movement, but exhibit abnormal postures and
spatial errors. Ideomotor apraxia is seen with lesions in the
dominant parietal cortex, in or around the area of the superior
marginal and angular gyrus
74
Conduction apraxia
The dominant feature of conduction apraxia is impairment in
imitation of movements. The localization of conduction apraxia is
not well defined
75
Ideational apraxia
Ideational apraxia is characterized by impairment in the
sequence of motions needed to carry out a specific movement.
When asked to pantomime pouring a glass of water and drinking
from it, patients with ideational apraxia will, for example, drink
from the cup before pouring water into it. Ideational apraxia is
seen in patients with bifrontal or biparietal dysfunction, as occurs
in neurodegenerative disorders.
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Dissociation apraxia
Disassociation apraxia is characterized by inability to execute a
movement on command, but with normal ability to imitate. It has
most commonly been reported to occur in the left hand in left
hemispheric language dominant patients who have left MCA
territory lesions.
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Conceptual apraxia
Conceptual apraxia is characterized by misconception of the
function of objects in the environment. For example, a patient with
conceptual apraxia might use a fork to eat soup, or may pretend to
use a screwdriver when asked to pantomime hammering a nail into
a wall. Conceptual apraxia is seen with diffuse neurodegenerative
processes, as well as with lesions in the nondominant hemisphere
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Dressing apraxia
Dressing apraxia localizes to the right parietal lobe. It often occurs
in the setting of a neglect syndrome.
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Wisconsin Card Sorting Test
Wisconsin Card Sorting Test can be used as a measure of
prefrontal cortical function. It requires the patient to arrange cards
based on a specific concept. It is a test of frontal lobe function, and
assesses visual conceptualization and set shifting
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Grooved Pegboard Test
Grooved Pegboard Test evaluates finger dexterity. The
patient is timed as he/she places pegs into small grooved holes in a
board. The grooves are oriented in different directions, requiring
the patient to rotate the peg in their fingers, which increases the
demands for distal dexterity. Right and left hands are performed
separately, and the patient’s time is compared to normative data
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Trail Making Test Part A Dan TMT B
Trail Making Test Part A times the patient as he/she
connects numbers on a page, and is a test of simple speed of
processing, visual search, and attention. The Trail Making Test Part
B requires the patient to connect consecutive numbers and letters,
and tests set shifting (shifting between numbers and letters) and
working memory (maintaining the correct sequence), in addition to
the demands of Trails A
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Random Cancellation Test
Random Cancellation Test, a measure of visual attention and
processing speed, assesses the ability to visually scan and identify
specific targets in a large array of similar items
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Clock-Drawing Test
Clock-Drawing Test, a test of visuospatial function but
also auditory comprehension, attention, and executive function, the
patient is asked to draw a clock (including the numbers) with the
hands set at a specific time
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Perbedaan dementia Dan delirium
Delirium affects mainly attention.
Dementia affects mainly memory. (Terutama recent memory). Atensi tidak terganggu sampai Dementia berat
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Virtual Reality treatment
Terapi utk mengatasi anxiety.
