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form activities, such as paying bills and managing medication become impaired from an early
stage.
1.5.2 Behavioral andPsychological
Symptoms ofDementia: BPSD
Behavioral and psychological symptoms such as
impaired motivation and emotion, delusion, hallucination, wandering behavior, agitation, and
aggression occur. Indifference, decreased spontaneity, and depression are also common. In
Alzheimer’s disease, delusions of robbery and
delusion of persecution are common, and characteristic interpersonal behaviors such as lack of
disease awareness and mending reactions are
observed. On the other hand, visual hallucination
is common in Lewy body dementia.
1.5.3 Others
Depending on the cause of cognitive impairment,
there are characteristic symptoms other than cognitive dysfunction, such as parkinsonism in Lewy
body dementia.
1.6 Clinical Examination
1.6.1 Psychological Test
Patients with cognitive complaints should
undergo a careful mental states examination. The
Mini-Mental State Examination (MMSE) is the
most widely used screening scale for cognitive
dysfunction in dementia, and a score of 23 or
lower is considered suspicious for dementia.
1.6.2 Blood Test
To differentiate cognitive dysfunction associated
with medical diseases, blood count, blood biochemistry, thyroid function, electrolytes, fasting
blood glucose, vitamin B12, folic acid, and serum
syphilis tests should be performed.
1.6.3 Neuroimaging
1. Brain MRI and CT: The rst step is to
exclude treatable dementia. The pattern of
atrophy and signal changes in the cerebral
atrophy are useful for distinguishing the cause
of dementia.
2. Single-photon emission tomography
(SPECT): Alzheimer’s disease is characterized by hypoperfusion in the posterior cingulate gyrus, precuneus, and parietal association
areas.
1.7 Diagnosis
The diagnosis of dementia is based on history,
physical and neurological examination, and
laboratory and neuroimaging ndings. Many
drugs that cause cognitive impairments, and it
is necessary to conrm the contents of medication. In particular, anticholinergic agents and
benzodiazepines are at risk of causing
dementia.
1.8 Treatment
Treatment of dementia aims to improve cognitive
function and quality of life (QOL), which are the
core symptoms. For behavioral and psychological symptoms of dementia (BPSD) such as paranoia and irritability, environmental adjustment
and non-pharmacotherapy may provide maximal
benets.
1.8.1 Drug Therapy
Three cholinesterase inhibitors, donepezil, galantamine, and rivastigmine, and an N-methyl-D-
aspartate (NMDA) receptor antagonist,
memantine, are available symptomatic medications for cognitive function in Alzheimer’s
disease.
1.8.2 Non-Drug Therapy
These include cognitive function training, cognitive stimulation, exercise therapy, music therapy,
and training in activities of daily living. Dental
treatment and oral care are also vital, and preventive and continuous oral hygiene management is
necessary.
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1.9 Prognosis
As the disease progresses, almost all memory is
impaired, and the patient eventually loses the
ability to perform self-care tasks such as dressing, eating, toileting, bathing, and understanding
and speaking. Basic motor skills are also lost, and
the patient eventually becomes bedridden. In the
terminal stage, the patient dies from complications such as malnutrition, dehydration, and
infections such as aspiration pneumonia [8].
1.10 Recent Findings
Many patients with dementia show eating behavior change, low nutrition, and weight loss due to
eating disorders and dysphagia. Therefore, it is
important to evaluate nutrition, prevent aspiration,
and review drugs, depending on the progress.
However, percutaneous endoscopic gastrostomy
(PEG) does not prolong long-term survival in
patients with severe dementia [9].
Diabetes mellitus, obesity in middle age,
hypertension, depression, hearing impairment,
and smoking are risk factors for the development
of dementia, and intervention in these areas is
expected to prevent the onset of dementia. In
addition, regular exercise and social participation
have been shown to have preventive effects [10].
Recently aducanumab, recombinant monoclonal
antibody directed against amyloid beta, is
approved by the US Food Drug Administration
(FDA) for the treatment of mild Alzheimer’s disease. At present, there is uncertainty about
whether patients benet clinically from aducanumab [11].
1.11 Notes fromDentistry
Perspective
TetsujiOkamoto,TomoakiShintani
1.11.1 Periodontitis andAlzheimer’s
Disease
The etiology of Alzheimer type dementia (hereafter referred to as Alzheimer’s disease) remains
unclear, and effective prevention and treatment
have not yet been established. There have been
many reports on the relationship between
Alzheimer’s disease and the oral cavity, and it has
been shown that “tooth loss” and “periodontitis”
are risk factors, each of which induces Alzheimer’s
disease by its own mechanism [12, 13]. Regarding
the relationship between tooth loss and Alzheimer’s
disease, it has been suggested that tooth loss
reduces chewing efciency and decreases blood
ow to the brain, causing cognitive dysfunction
[13]. Oue etal. found that the maxillary bilateral
molar extraction group showed a decrease in cognitive function and a signicant decrease in the
number of neurons in the hippocampus compared
with the non- extraction group, but there was no
difference in the deposition of amyloid β protein
(Aβ) in the brains of the two groups using the
Alzheimer’s disease transgenic mice [14].
On the other hand, periodontitis is a chronic
infection caused by periodontopathic bacteria,
and it has been reported that periodontitis is a risk
factor for systemic diseases such as diabetes mellitus, myocardial infarction, atherosclerosis, preterm and low birth weight, endocarditis, aspiration
pneumonia, and rheumatoid arthritis [15]. DNA
of Porphyromonas gingivalis (P. g ), a periodonto-
pathic bacterium, has been detected in the placenta of mothers who delivered preterm or low
birth weight babies and in atherosclerotic plaques
in the aortic wall of patients with atherosclerosis
(Fig. 16.1) [16]. Furthermore, bacterial components of P. g have been detected in the liver parenchyma of patients with nonalcoholic steatohepatitis
(NASH), suggesting that they may be involved in
the progression of NASH.Since microglia, a type
of macrophage, are activated in the brains of
patients with Alzheimer’s disease, Alzheimer’s
disease is considered a chronic inammation of
the brain [17], and many studies have investigated
its relationship with periodontitis.
Serum antibody titers against Fusobacterium
nucleatum and Prevotella intermedia were
increased in Alzheimer’s disease patients [18],
and the presence of lipopolysaccharide (LPS)
from P. g in the brain was conrmed [19, 20]. In
the Alzheimer’s disease transgenic mice infected
with P.g , cognitive function is further reduced
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Fig. 16.1 Organs and
diseases in which P. g
bacteria were detected
Oral
P.gingivalis
and the deposition of Aβ in the brain is increased
[21]. In addition, periodontopathic bacteria and
bacterial-derived LPS activate macrophages, and
inammatory mediators such as TNF-α, IL-1,
IL-6, and CRP produced by macrophages in the
periodontal region are transported to the brain via
the bloodstream and induce inammatory reactions in neurons, which may exacerbate the
pathogenesis of Alzheimer’s disease [22].
Although periodontopathic bacteria cannot
invade the brain parenchyma because of the
blood-brain barrier (BBB) in the brain, it is
thought that periodontopathic bacteria may reach
the brain by increasing the permeability of the
BBB due to inammatory cytokines in the blood
and aging of cerebral blood vessels [23]. After
inammatory cytokines and periodontopathic
bacteria reach the brain parenchyma, abnormal
aggregation and deposition of Aβ induces neuronal apoptosis, resulting in the appearance of
symptoms of Alzheimer’s disease [17]. It has
been reported that P. g exist in the brains of
Alzheimer’s disease patients and that DNA of P. g
exists in spinal cord secretions, and gingipains,
proteolytic enzymes produced by P. g , have been
detected in the brains of Alzheimer’s disease
patients [24]. In the brains of patients with
Alzheimer’s disease, tau and ubiquitin, proteins
strongly associated with Alzheimer’s disease,
were found to be present in large amounts [24],
and clinical studies of the molecular target therapy targeting gingipains for the disease have
Brain: Alzheimer's disease
Heart: arteriosclerosis
Liver: nonalcoholic steatohepatitis
Placenta: premature birth and low birth weight
already been initiated [24]. On the other hand, it
was found that the number of bacteria of the
genus Bacteroides was signicantly lower in the
intestinal microora of elderly patients with
dementia than that of non-demented elderly
patients [25].
Thus, periodontitis is considered to be a risk
factor for Alzheimer’s disease, and treatment of
periodontitis may prevent Alzheimer’s disease or
delay the progression of the disease.
1.11.2 Dysphagia inPatients
withAlzheimer’s Disease
With the progression of Alzheimer’s disease,
memory impairment, impaired judgment, and
disorientation, which are the main symptoms of
the disease, progress, and it is difcult to recognize how to eat food and what food is offered. As
dementia progresses and ADL (Activities of
Daily Living) decline signicantly, swallowing
function declines and nutritional status deteriorates. A characteristic feature of Alzheimer’s disease is that the onset of eating and deglutition
disorders is different. In addition, as Alzheimer’s
disease becomes more severe, patients may
require assistance to wear dentures, or they may
refuse to wear or use dentures. Denture refusal
not only makes it difcult to consume food, but
also leads to deterioration of masticatory function and aspiration, which in many cases leads to
deterioration of nutritional status and
dehydration.
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1.11.3 Dental Treatment andOral Care
forPatients withAlzheimer’s
Disease
Dental treatment in patients with Alzheimer’s disease should be planned in accordance with the progression of dementia [26]. In the early stage,
patients with Alzheimer’s disease can be treated
with conventional dentistry, including tooth extraction, endodontic treatment, and prosthetic treatment. In the middle stage of the disease, the patient
has difculty in following detailed instructions and
in taking long dental treatments. In addition, masticatory dysfunction is observed, and assistance during meals and changes in eating patterns become
necessary. In the latter stage, communication
becomes difcult, and not only normal dental treatment but also denture cleaning and oral self-care
cannot be performed, and oral hygiene deteriorates,
so the intervention of oral care is essential.
In addition, to prevent aspiration pneumonia,
oral care is necessary to reduce the number of
oral bacteria as much as possible. Furthermore,
nutritional management is also important because
dentures become difcult to wear. In order to
make oral care as smooth as possible, it is important to perform it in a familiar environment and
with dental staffs, and to talk to the patient in a
way that gives a sense of security. Patients with
impaired swallowing function should receive oral
care while taking care to avoid aspiration. Patients
who cannot control their body movements should
not be forced to perform oral care.
Although there are individual differences in
Alzheimer’s disease, it is a progressive disease and
oral care is essential for many patients. Therefore,
when planning treatment, it is important to intervene
to create an oral environment that facilitates better
oral care, such as preserving residual root teeth as
much as possible and avoiding the fabrication of
dentures that are difcult to put on and take off.
2 Epilepsy [27–29]
KazuhiroMuramatsu
2.1 What Is Epilepsy?
Epilepsy is a chronic brain disease that causes
repetitive seizures of the brain due to the overex-
citement of nerve cells in the cerebrum. The seizures are sudden and cause unusual physical
symptoms and changes in consciousness, movement, and sensation. If there are obvious convulsions, epilepsy is the most likely cause. In
addition to convulsions, epilepsy can cause a
variety of other symptoms, such as lightheadedness, body twitching, and moving around while
unconscious. Epilepsy is characterized by recurrent episodes. Various tests, mainly electroencephalography, are necessary to conrm the
diagnosis.
2.2 Epidemiology
Epilepsy is one of the most common central
nervous system diseases, along with
Alzheimer’s disease and cerebrovascular disease. The prevalence of epilepsy is 4 to 8 per
1,000 of the general population in developed
countries. In Japan, the number of patients is
estimated to be 650,000 to 900,000. The incidence of epilepsy is about 45 cases per 100,000
people per year in developed countries. The
incidence of epilepsy has been shown to be
higher in infants and the elderly. It is estimated
that there are about 300,000 people with epilepsy in the elderly in Japan.
2.3 Classication
Classication of epileptic seizures is essential for
subsequent patient handling, testing, and selection of antiepileptic drugs, and the International
League Against Epilepsy (ILAE) classication is
used. Until now, the 1981 classication for epileptic seizure types and the 1989 classication
for epilepsy, epilepsy syndromes, and related seizure disorders have been widely used, but in
2017, the ILAE proposed a new epileptic seizure
and classication (Figs. 16.2 and 16.3). The
ILAE proposed that epileptic focal epilepsy
should be referred to as focal epilepsy when the
epileptic focus is in neural circuits in one hemisphere and generalized epilepsy when the epileptic focus is in neural circuits spanning both
hemispheres.
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Fig. 16.2 ILAE 2017 Classication of seizure types (reproduced with permission from [27])
2.4 Interview forEpilepsy
Diagnosis
Gathering sufcient information and witnessing
the seizures are most helpful in diagnosing epilepsy. Although the chief complaint is often a
convulsive seizure (and sometimes a nonconvulsive seizure), more than one seizure is usually
necessary to diagnose epilepsy. Patients and seizure witnesses may provide information on seizure frequency, seizure circumstances and
triggers (e.g., photosensitivity), symptoms before
and during seizures (physical and mental symptoms and disturbance of consciousness), persistence of symptoms, symptoms following seizures,
presence of trauma, bite tongue, urinary incontinence, headache and muscle pain after seizures,
age of rst attack in patients with multiple seizures, seizure and changes/transitions in seizure
type, last seizure, relationship between seizures
and wakefulness/sleep, etc.
2.5 Diseases that Need
tobeDierentiated
fromEpilepsy (Table16.3)
Neurally mediated syncope/psychogenic nonepileptic seizures account for 40% of patients presenting to the emergency department with
sudden-onset loss of consciousness, followed by
epilepsy in 29% and cardiogenic seizures in 8%.
To diagnose epilepsy, it is important to investigate
the cardiovascular cause. The characteristic feature of syncopal seizures is that they are not
accompanied by altered consciousness, fatigue, or
malaise. The overall risk of developing epilepsy
in patients who have an acute seizure within
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Fig. 16.3 ILAE 2017 Framework for classication of the epilepsies (three levels of epilepsy diagnosis) (reproduced
with permission from [28])
Table 16.3
epilepsy
Fainting (neuromodulatory, cardiogenic, etc.)
Psychogenic non-epileptic seizure
Hyperventilation and panic attacks
Stroke (cerebral infarction, cerebral hemorrhage),
transient ischemic attack
Sleep-related disorders (abnormal REM sleep behavior,
non-REM parasomnias)
Acute poisoning (drugs, alcohol), drug withdrawal,
alcohol withdrawal
Acute metabolic disorder (hypoglycemia, tetany)
Acute renal failure
Head trauma (within 1week)
Involuntary movements (tics, tremors, myoclonus,
paroxysmal dyskinesia, etc.)
Paroxysmal ataxia
Diseases that should be differentiated from
1week of head injury is about 25%. Alcohol withdrawal may cause convulsive seizures.
2.6 Procedure fortheDiagnosis
ofEpilepsy [29]
Electroencephalography (EEG) (including photic
stimulation, hyperventilation, and sleep) should
be recorded for the rst unprovoked epileptic seizure. Sleep-activated EEG can increase the frequency of epileptic discharge recordings. If
necessary, neuroimaging and simultaneous
video-EEG recording should be performed.
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In the diagnosis of epilepsy, EEG is the most
useful test, but it may not be possible to make a
diagnosis with only one conventional EEG, and
multiple EEGs, including sleep activation, are
necessary. Prolonged video- EEG monitoring is
useful in the denitive diagnosis, typing, and
localization of epilepsy.
Neuroimaging studies (MRI or CT) should be
performed to diagnose epilepsy. MRI is particularly useful when focal-onset epilepsy is suspected. When an MRI or CT scan of a patient
with a rst unprovoked seizure shows organic
lesions suggestive of stroke, central nervous system infection, or traumatic brain injury, the
patient should be diagnosed as epilepsy even if it
was the rst seizure, because of the high risk of
recurrence.
2.7 What toDo During
anEpileptic Seizure
First, it is important to ensure safety and observe
seizure symptoms. It is necessary to conrm that
the place where the seizure occurred is not dangerous and that there are no dangerous things around,
and depending on the situation, it may be necessary
to assist the patient or keep away from dangerous
things. Observation of seizure symptoms is the
basis for the “symptomatic diagnosis” of epilepsy.
For cases of vomiting during or after seizure,
there is also impaired consciousness and the vomit
tends to get stuck in the throat, the patient should be
placed on their side so that vomit can go out. After
a seizure, the patient becomes sleepy, so let him
sleep for a while. Patients with normal seizures
recover after 30min to 1h of sleep, or 2h at most.
Seizures that last more than a certain length of
time or are repeated even if they are short and
without recovery of consciousness are called status epilepticus, and treatment should be started
immediately.
2.8 Drug Treatment ofEpilepsy
As a rule, antiepileptic drug therapy should not
be initiated for the rst unprovoked seizure.
Patients with neurological abnormalities, electro-
encephalographic abnormalities, brain imaging
lesions, or a family history of epilepsy are more
likely to have recurrent seizures and should be
considered for treatment.
Antiepileptic drug therapy is usually initiated
as a single agent. The choice of drug should be
based on the seizure type and the diagnosis of
epilepsy, taking into account the patient’s individual condition. Carbamazepine, lamotrigine,
and levetiracetam are recommended as rst-line
agents in patients with focal-onset epilepsy, while
valproate is recommended as rst-line therapy in
patients with generalized-onset epilepsy.
If the patient is well controlled with medication, all dental procedures can be performed
almost normally. Epinephrine-containing cannabis is not a problem. Problems arise in patients
who are off medication or who have complications such as infection or fatigue.
2.9 Notes fromDentistry
Perspective [30–34]
TadashiKawai
2.9.1 Oral Cavity ofEpileptic Patients
Patients with epilepsy are often treated with single
or multiple medications, and patients taking phenytoin may develop drug-induced gingival hyperplasia, with an incidence of about 50%. It is thought
that phenytoin increases the proliferation of gingival broblasts, increases the synthesis of extracellular matrix by gingival broblasts, and decreases
their resolving power. Gingival hyperplasia can be
improved by oral cleaning. Still, if symptoms are
marked, the dentist should ask the patient’s physician to change the medication, and if this is difcult, a gingivectomy may be performed.
2.9.2 Conrmations Before Dental
Treatment
Before dental treatment, the dentist should consult with the patient’s physician for details of
the patient’s condition, history, current condition, medications, and precautions for dental
treatment. Information on the severity of the
epileptic seizures is also necessary, such as
whether they are minor seizures with a brief loss
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of consciousness or major seizures leading to
convulsions (seizures). The presence or absence
of other comorbidities should also be conrmed.
Even if the patient claims that his or her symptoms have calmed down, dental treatment
involves a variety of invasive procedures, and if
we believe the patient’s words and proceed with
treatment without paying attention to the
patient’s condition, the invasive procedures may
trigger an epileptic seizure and cause serious
problems. Therefore, dental treatment should be
performed with care to prevent epileptic seizures. The presence or absence of epileptic aura
and how to respond to seizures at home should
also be conrmed.
2.9.3 Precautions forDental
Treatment
A variety of invasive procedures can be expected
at the beginning of dental treatment. Even if the
treatment has not started, a long waiting time in
the waiting room may induce epileptic seizures
due to nervousness about dental treatment.
Therefore, it is advisable to avoid a long waiting
time after the patient arrives at the clinic. The
patient’s physical condition should be checked
before the treatment begins. Check that the
patient is tired or not, and that they have not forgotten to take the medicine. If there are any
problems, it is advisable to postpone the treatment. Attention should also be paid to the environment during dental treatment. Loud noises,
such as dropping objects on the oor and light
stimulation can be very stressful. Proceeding
with treatment without talking to the patient can
also cause anxiety and distress, and should be
treated appropriately. With regard to local anesthetics, there are no contraindications to epinephrine or concomitant use of antiepileptic
drugs, but it is advisable to check other drugs,
such as psychotropic drugs, that are prescribed
concomitantly. Concerning prescription drugs
from dentists, concomitant use of acetaminophen in patients taking phenytoin is cautioned
because of the increased risk of liver
dysfunction.
2.9.4 What toDo During anEpileptic
Seizure
Even if the above information is considered during treatment, seizures may still occur because
dental treatment itself is invasive for the patient.
If the patient is unresponsive or has a seizure,
stop treatment and observe the patient until they
regain consciousness in a few seconds. After that,
give only rst aid and postpone treatment. If a
grand mal occurs, as many people as possible
should assemble to prevent the patient from falling off the dental unit. Administer diazepam, if
available. Intravenous injection is preferable, but
intramuscular injection is also acceptable if convulsions make it difcult. Convulsions often subside in a few minutes, and the patient should be
kept under control until then. Because the patient
is not breathing spontaneously, the oxygen saturation level (SpO2) drops to about 80%. Oxygen
may be administered during convulsions, but it
may not be effective because spontaneous breathing is not stable. In fact, it is better to administer
oxygen after the patient regains consciousness
because of the fatigue caused by the convulsions.
After the seizure subsides, the patient should rest
for a while, and when consciousness is clearly
restored, treatment should be terminated and the
planned treatment should be postponed.
For subsequent treatment, the reasons for the
seizures should be reviewed and analyzed. If there
is an obvious cause, it should be noted in the next
treatment. It is also advisable to report the seizure
to the patient’s doctor. The doctor may consider
changing the medication to control the seizures.
3 Parkinson’s Disease
KanakoYamahara,TetsuyaMaeda, and
YasuoTerayama
3.1 Introduction
Parkinson’s disease (PD) is the second most common neurodegenerative disease next to Alzheimer’s
disease (AD). A neurodegenerative disease is a dis-
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order in which a specic group of neurons in the
brain and spinal cord are damaged and lost. In AD,
cortical neurons in the cerebrum are affected,
whereas in PD, dopaminergic neurons in the substantia nigra of the midbrain are selectively degenerated and lost. As a result, the striatal level of
dopamine decreased, resulting in dysfunction of
the basal ganglia circuits and the emergence of
various movement disorders. The cause of PD
remains unknown, but the involvement of genetic
and environmental factors is known to be important. The prevalence of PD in Japan is 100 to 180
per 100,000 people, but increases with age and is
estimated to be 1in 100 for people aged 70years or
older. The number of patients with PD continues to
increase with the aging of society, and it is predicted that the global PD population will exceed 13
million by 2040 at the lowest estimate [35].
3.2 Pathogenic Factors
PD is a sporadic disease in general and usually
develops in the 60s. Those with onset age at 40
or younger are associated with genetic abnormalities, and hereditary PD accounts for about 10%
of all. Pathologically, PD is characterized by the
presence of intracellular inclusions called Lewy
body in the residual dopaminergic neurons in the
substantia nigra pars compacta. The main component of Lewy body is α-synuclein, which is
formed by abnormal aggregation in the presence
of genetic and environmental risks. α-synuclein
has been shown to propagate between neurons
and is thought to be a key molecule involved in
the onset, progression, and treatment of PD.
3.3 Parkinson’s Disease Clinical
Syndrome
PD is a movement disorder characterized by
motor symptoms. However, it is clinically considered a systemic neurological syndrome that
also presents with non-motor symptoms. Cardinal
motor symptoms include (1) tremor at rest:
4–6 Hz constant involuntary movements of ngers, hands, arms, and legs; (2) rigidity: an abnormal increase of muscle tone evoked by passive
movement of limb joints; (3) akinesia and bradykinesia: small voice, poor facial expression, and
decrease of body spontaneous movements which
takes time to perform daily activities; and (4)
postural instability: leading poor postural balance
and frequent fall. Due to these symptoms, the
patient has a lack of facial expression, leans forward, and walks in a small, unsteady manner. The
tremor tends to disappear during movement and
to increase with tension and anxiety. These symptoms respond well to anti-parkinsonian agents
and can be maintained with activities of daily living if appropriate treatment is initiated. However,
as the disease progresses and becomes more
severe, patients may require assistance in turning
and rising from bed, and dysarthria and decreased
swallowing function may be observed. Since
risks of aspiration pneumonia and bone fracture
due to falls increases, prevention through oral
care and rehabilitation is important.
On the other hand, PD has a variety of non- motor
symptoms as shown in Table 16.4 [36], which are
difcult to treat in clinical practice. The most common symptoms in the early stages of the disease are
constipation, sleep disturbance, depressive mood
Table 16.4 Indications of nonmotor symptoms (cited
from [36])
• Neuropsychiatric symptoms
Depression and depressive symptoms
Anxiety and anxiety symptoms
Apathy
Psychosis
Impulse control and related disorders
Dementia
Cognitive impairment (other than dementia;
mainly mild cognitive impairment)
• Autonomic dysfunction
Drooling
Orthostatic hypotension
Urinary dysfunction
Erectile dysfunction
Gastrointestinal dysfunction
Excessive sweating
Disorders of sleep and wakefulness
Sleep fragmentation and insomnia
Rapid eye movement sleep behavior disorder
Excessive daytime sleepiness
• Others
Pain
Fatigue
Olfactory dysfunction
Ophthalmologic dysfunction
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disorders, fatigue, hyposmia, and pain. About 10
years after the onset of PD, orthostatic hypotension
appears as a symptom of autonomic failure and the
frequency of dizziness and falls increases. Even if
there are no subjective symptoms, systolic blood
pressure may drop 30 to 50mmHg after repositioning or urinating. Sudden repositioning should be
avoided, especially in dehydration cases. Cognitive
decline is also a common symptom of PD. In the
early stage, cognitive processing speed is mainly
affected and making plans and recalling words
become difcult. Gradually, cortical symptoms such
as memory disorder, decreased attentiveness, and
executive function impairment become apparent.
After dementia becomes apparent, clear visual hallucinations of people and small animals are often
experienced. These non-motor symptoms are known
to deteriorate the quality of life (QOL) in PD patients.
Therefore, management of non-motor symptoms are
clinically important as well as motor symptoms.
3.4 Diagnosis
In PD, clinical examinations including blood
tests and brain MRI are not abnormal. These are
performed to exclude other diseases with similar
symptoms to PD.Multiple system atrophy, progressive supranuclear palsy, and corticobasal
degeneration are well known as important differential diagnoses of PD.In contrast to PD, these
diseases often have a short period of time until
gait disturbance and easy falling appear. Clinical
course is important for diagnosis, and neuroimagings used with nuclear medicine, such as
MIBG cardiomyography and dopamine transporter scintigraphy, are also employed
(Fig.16.4a–d). The most important practical difference between PD and other movement disorders with parkinsonism is the response to
dopaminergic agents. Clear and dramatic benecial response to the initial therapy using with
Fig. 16.4 MIBG myocardial scintigraphy (upper panel)
and dopamine transporter SPECT (lower panel):
Parkinson’s disease patient on the left and normal subject
on the right. Decreased accumulation in the patient with
Parkinson’s disease, respectively
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