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Table 16.5
ease and impairment of life
Hoehn & Yahr’s severity
classication
I Unilateral disorder with
II It is a bilateral disorder
III The patients have obvious
IV There is a marked decrease
V The patient becomes unable
Classication of severity of Parkinson’s dis-
Ministry of Health,
Labour and Welfare’s
classication of
functional disability
in daily life
(Research Group for
Abnormal Motor
Diseases)
The patient needs
unilateral tremor and
muscle stiffness. It is a mild
case
with postural changes but
without postural instability.
There is some disability in
daily life and employment
due to the bilateral presence
of muscle rigidity and
bradykinesia to akinesia
gait disorder. They have
postural instability, and fall
easily when changing
direction but can walk.
They are able to live
without assistance and can
work depending on their
occupation, although their
activities are limited
in activities of daily living,
such as standing and
walking, and the ability to
work is lost. It is difcult to
live only by oneself
to stand and is wheelchairbound or bedridden with
assistance
little assistance in
daily life and
hospital visits
Partial assistance is
required for daily life
and hospital visits
The patient needs
full assistance in
daily life and is
unable to walk or
stand up by himself
L-dopa is supportive to diagnose PD. Clinical
severity of PD is usually evaluated by Hoehn &
Yahr staging (Table16.5), which is a simple and
standard assessment method in the world.
3.5 Treatment
Treatment of PD is classied into medical, surgical, and exercise therapy. There is no curative
treatment for PD, and the most common treatment is dopamine replacement therapy.
The mainstay of medical therapy is L-dopa and
dopamine agonists. L-dopa is the most effective
agent, but its duration of action is short, and longterm administration is associated with motor complications (wearing-off phenomenon, dyskinesia).
Therefore, concomitant therapy with dopamine
agonists is common, which have variable formulations, including oral pills, subcutaneous self-injection, and transdermal patch. All of them can be
selected according to the patient’s lifestyle. Since
sleep attacks and psychiatric symptoms have been
reported as major side effects, it is recommended
that patients with cognitive decline or suspected
impulse control disorders refrain from using the
drug. Selective monoamine oxidase B (MAO-B)
inhibitors, catechol- o-methyl transferase (COMT)
inhibitors, adenosine A2A receptor antagonists, and
zonisamide as activator of dopamine system are
also used as adjunctive agents with L-dopa. The
motor symptoms respond well to dopamine
replacement therapy in the early stage, and honeymoon period follows in which the primary symptoms become less prominent. However, as the
disease progresses, the effectiveness of the antiparkinsonian drugs are ameliorated and symptomatic uctuation (wearing-off phenomenon) and
hyperkinetic abnormal involuntary movements
(dyskinesia) may emerge. These are dened as
motor complications and the clinical phase with
them is dened as the advanced stage. In the
advanced stage, therapeutic strategies such as
increasing the frequency of medication or usage of
a longer-lasting effect are necessary to maintain
the motor complications.
Malignant syndrome is the most important
issue in patients using anti-parkinsonian drugs.
PD patients usually take multiple drugs in combination. Abruptly discontinuation of their drugs
due to poor physical condition or fasting periods
associated with surgery or examination may
result in the development of serious symptoms
such as high fever, disturbance of consciousness,
rigidity of extremities, and rhabdomyolysis.
When a fasting period is required for examination, treatment, or surgery, supplementation with
L-dopa by intravenous infusion or concomitant
use of transdermal patch should be considered to
prevent this malignant syndrome.
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Functional surgery should be considered for
patients with advanced PD who have uncontrollable
motor complications with anti-parkinsonian medications. Practically, eligible conditions for surgical
treatment are patients who do not respond to antiparkinsonian medication even for a short period,
who are independent during on state but cannot get
up and walk without assistance when off state. In
Japan, deep brain stimulation and intraduodenal
L-dopa carbidopa intestinal gel therapy are the two
options, called device-assisted therapy in terms of
treatment using medical equipment.
In recent years, dopaminergic neuronal cell
transplantation derived from induced pluripotent
stem (iPS) cells and nucleic acid therapy targeting the SNCA gene encoding an α-synuclein are
noticed as attracting treatments, which also
involves surgical procedures. In the former treatment, iPS-derived dopaminergic progenitor cells
are stereotactically injected into the putamen to
replace lost dopaminergic neurons. The latter is a
treatment using a nucleic acid drug called AmNAmodied antisense nucleic acid, which has been
reported to suppress the accumulation of
α-synuclein in brain cells by inhibiting the
expression of the SNCA gene. Treatment development is constantly underway, and these studies
are also highly promising areas.
Finally, exercise therapy is essential for the
maintenance of motor function, because it can be
performed at any stage of the disease, from early
onset to advanced stages, in parallel with pharmacotherapy and surgical treatment. In recent years,
clinical studies have been conducted and scientic evidence for the efcacy of exercise therapy
has been accumulated. However, motivation is
often low in PD patients, and it is important to
inspire patients to continue exercise therapy.
3.6 Notes fromDentistry
Perspective [37–39]
toms such as decreased chewing and swallowing
functions and sialorrhea appear in the oral cavity.
The oral environment is also affected by oral medications. When anticholinergic drugs, which are
parasympathomimetic drugs, are prescribed, their
effects suppress saliva secretion at rest, resulting in
xerostomia. This may increase the risk of dental
caries and periodontal disease, and may be accompanied by other oral mucosal diseases and mucosal damage due to denture incompatibility. In
patients with advanced disease, involuntary movements (oral dyskinesia) such as lip gagging and
tongue twisting may occur in the mouth.
3.6.2 Conrmations Before Dental
Treatment
Prior to dental treatment, the patient’s physician
should be consulted about the details of the disease, the patient’s history, current condition,
medications, and precautions for dental treatment. Depending on the severity of Parkinson’s
disease, there is a limit to the content of dental
treatment that can be performed. Even patients
with Parkinson’s disease who have relatively little difculty in daily life or who require only
minor assistance may have diurnal variation in
symptoms. The presence of other complications
such as cerebrovascular disease, malignant
tumors, and infections should also be checked.
3.6.3 Precautions forDental
Treatment
In theTreatment Room
Patients with Parkinson’s disease may have difculty moving due to movement disorder, and it is
necessary to pay attention to their feet when
moving around in the clinic room and transferring to the unit. Patients with Parkinson’s disease
may also have difculty in conversation, so it is
necessary to communicate with them in a relaxed
manner to avoid stress.
TadashiKawai
3.6.1 Oral Cavity ofPatients
withParkinson’s Disease
Patients with Parkinson’s disease have difculty
moving their bodies smoothly, and various symp-
Clinic Hours
Because of the lack of efcacy of oral medications
for Parkinson’s disease (wearing-off phenomenon), once diurnal variation in symptoms has been
identied, treatment should be performed to the
time of day when the medication is most effective.
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The morning hours are often chosen. It is not
advisable to carry out treatment for too long, so
treatment should be completed promptly.
Local Anesthetics
In patients taking levodopa-containing drugs,
epinephrine may induce marked increases in
blood pressure and tachycardia because the
metabolism of epinephrine with a catechol group
is inhibited. Monoamine oxidase inhibitors and
catechol-O-methyltransferase inhibitors also
induce elevated blood pressure and tachycardia
with epinephrine. Patients taking dopamine
receptor stimulators should be cautioned against
concomitant use of epinephrine because of its
vasoconstrictive effects and blood pressure
increasing effects, although the mechanism of
action is not clear. Since many Parkinson’s
patients are taking these drugs, it is advisable to
avoid epinephrine-containing local anesthetics.
During Dental Treatment
Orthostatic hypotension may occur in 20 to 30%
of patients with Parkinson’s disease who are taking medication. Therefore, patients with
Parkinson’s disease should move slowly when
raising the dental unit during treatment. The
patient should be careful about aspiration because
of dysphagia. Be careful about vacuuming during
treatment with water. In patients with signicant
dysphagia, it is advisable to set the angle of the
dental unit at 45° to prevent aspiration of saliva or
water stored in the mouth. Since the patient’s
facial expression may be poor, check their condition by talking to them as appropriate. During
treatment, blood pressure and arterial oxygen
saturation (SpO
of uctuations in blood pressure and the effect of
aspiration on respiration.
) should be monitored because
2
3.6.4 Oral Management
Although dental treatment is not easy due to the
nature of the disease, regular oral management
every 3 to 4 months is necessary. If oral management is inadequate, occlusion may collapse due
to the high risk of dental caries and periodontal
disease, and oral nutritional intake may become
difcult due to pain caused by oral mucosal disease. This may lead to weight loss. In addition, in
patients with advanced symptoms and marked
akinesia, aspiration pneumonia may occur
repeatedly.
The pathogenesis of Parkinson’s disease
should be understood, and dental treatment
should proceed with consideration to changes in
the oral environment and the resulting effects on
the whole body.
4 Amyotrophic Lateral
Sclerosis [40, 41]
SatoshiOkada
4.1 Concepts andDenitions
Motor neurons include lower neurons from the
brain stem motor neurons and anterior horn cells
of the spinal cord to skeletal muscles, and upper
neurons that travel through the pyramidal tract
from the motor area of the cerebral cortex and
connect to the lower neurons. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease in which both higher and lower motor
neurons are progressively impaired. The skeletal
muscles of the whole body are damaged, resulting in marked muscle weakness and atrophy. The
disease is often solitary, but it may occur
familial.
4.2 Pathophysiology
Although the etiology of sporadic ALS is still
unclear, it has been postulated that TDP-43 protein accumulates in the cytoplasm of motor neurons and is involved in RNA dysfunction. In
addition, glutamate-induced excitotoxicity, mitochondrial abnormalities, axonal transport disorders, and oxidative stress have been proposed to
be involved.
In familial cases, causative genes such as
SOD1, FUS, TARDBP, C9ORF72, optineurin,
UBQLN2, and ERBB4 have been identied.
Among these, SOD1 is the most common,
accounting for about 20%. It is not unusual for
phenotypic differences to occur even within the
same family.
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4.3 Epidemiology
The prevalence is 7 to 11 per 100,000 population,
and the incidence is 1.1 to 2.5 per 100,000 population. The male to female ratio is 3:2, with a
slightly higher incidence in males. The age of
onset is usually in the 60s to 70s. Familial ALS
accounts for 5% to 10% of cases.
4.4 Symptoms
4.4.1 Subjective Symptoms
Muscle weakness in all four limbs, dysarthria,
and dysphagia appear and progress. In the initial
stage, it is commonly observed muscle weakness on one side of the hand or upper limb. It
becomes difcult to use chopsticks and writing
becomes poor. In many cases, the inability to
open the lid of a plastic bottle is noticed.
Dysarthria and dysphagia may be the rst symptoms. The onset of lower extremity disease is
often noticed by difculty in walking or climbing of stairs. Muscle atrophy and weakness
extend to the extremities, trunk, and globe, and
the patient becomes bedridden. In addition,
respiratory muscle dysfunction leads to respiratory failure and death, or the need for a
ventilator.
4.4.2 Objective Symptoms
The presence of both upper and lower neuron
signs is essential for a denitive diagnosis. The
upper neuron signs include increased tendon
reexes in the extremities, spasticity, and pathological reexes such as clonus and Babinski’s
sign (Table 16.6). Lower neuron signs include
muscle atrophy and weakness, often asymmetrical in appearance. Fasciculation is a characteristic sign and is often observed at rest in muscle
groups with progressive atrophy, such as the
quadriceps muscle, shoulder girdle muscles,
intrinsic muscles, and tongue. In addition, dysarthria, dysphagia, and atrophy of the tongue are
observed due to bulbar palsy. Decreased cognitive function is another symptom that should be
noted. About half of the patients have cognitive
decline detectable by neuropsychological exami-
Table 16.6 Upper and lower neuron signs
Upper neuron
sign
Muscle weakness Advanced Slight degree
Muscle atrophy Advanced Without
Clumsiness Advanced Slight degree
Fasciculation Existence (at
Muscle tension Decreased Accelerated
Tendon reex Decreased or
Pathologic reexes
of the lower
extremities
the present
moment)
absent
Without Occasionally
Lower neuron
sign
Without
Accelerated
appears
nation. Some patients are diagnosed as having
frontotemporal dementia due to signicant cognitive decline. Negative symptoms include ocular
motility disorder, sensory disturbance, and rectovesical disturbance; however, even in the late
stage, the extraocular muscles, anal sphincter,
urinary muscles, cardiac muscles, and smooth
muscles are usually unaffected, and bedsores do
not occur.
4.5 Clinical Examination
4.5.1 Needle Electromyogram
It is an important test to identify disorders of the
lower motor neurons. Acute denervation ndings
include brillation potentials, fasciculation
potentials, and positive sharp waves. Chronic
denervation ndings include increased amplitude, polyphasic motor units, and prolonged
duration.
4.5.2 Peripheral Nerve
ConductionTest
A decrease in the amplitude of compound muscle
action potentials and a decrease in the frequency
of F waves may be observed. This is important to
rule out demyelinating neuropathy.
4.5.3 MRI
T2-weighted images of the head may show high
signal in the pyramidal tract and low signal in the
motor cortex. However, the positive rate is not
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high. MRI of the spinal cord is useful in differentiating cervical spondylosis.
4.6 Classication
As mentioned above, the onset type is sporadic
and hereditary. It can be divided into the following three groups according to the degree of
impairment of the upper motor neurons and lower
motor neurons. (1) Classical type: the upper and
lower motor neurons are damaged to the same
degree. (2) Progressive muscular atrophy type:
almost only lower motor neurons are affected,
and muscle atrophy and weakness are observed,
but no increased tendon reexes or pathological
reexes as signs of upper motor neurons are
observed. The differentiation from the adult form
of spinal muscular atrophy can be difcult. (3)
Primary lateral sclerosis type: almost all upper
motor neurons are affected, and there is no muscle atrophy or weakness.
also recommended. As ALS progresses, respiratory
failure may occur due to respiratory muscle damage. Noninvasive positive pressure ventilation
(NPPV) and tracheostomy positive pressure ventilation (TPPV) are available as ventilatory therapies, and the survival time of TPPV patients (mean
49.1 months) is signicantly longer than that of
non-TPPV patients (mean 35.8months).
4.8 Recent Findings
Research is being actively conducted to develop
more effective therapies; as of June 2019, clinical
trials of several drugs are underway, including a
new ALS treatment candidate found by a drug
screening approach using patient-derived iPS cells.
4.9 Notes fromDentistry
Perspective
TakaakiKamatani
4.7 Treatment
There is still no fundamental treatment for the disease. The effectiveness of currently available drugs
is limited, and symptomatic treatment and nursing
care are the mainstays of treatment. Riluzole and
edaravone have been used to slow the progression
of the disease. Riluzole is thought to have a protective effect on neurons mainly by inhibiting glutamate-induced excitotoxicity. Riluzole has a limited
effect, prolonging survival by only 2 to 3months.
In addition, edaravone, a free radical scavenger,
was covered by insurance in 2015in Japan, which
has been shown to have an inhibitory effect on the
progression of the early stages of the disease. Many
ALS patients experience pain. The causes include
painful muscle spasms, spasticity, contractures,
pressure from immobility, and psychological factors. Antiepileptic drugs, muscle relaxants, and
nonsteroidal anti-inammatory drugs are used, and
morphine is used when these drugs are not effective. Dysphagia may cause sialorrhea. Tricyclic
antidepressants may be effective. The use of a lowpressure continuous aspirator dedicated to saliva is
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease rst described by Charcot in
France in 1869, characterized by rapid symptom
progression and an average survival of 2 to 5
years. It is designated as an intractable neurological disease in Japan [42].
About one quarter of ALS patients are said to
have bulbar palsy type, in which the initial symptoms are dysarthria and eating disorder caused by
the dysfunction of the IX to XII cerebral nerves.
Patients may not be diagnosed even if they visit
multiple medical institutions with the main complaints of difculty in speaking and swallowing.
The diagnosis of ALS requires a differential diagnosis based on many professional examinations
in the eld of neurology, including motor neuron
disorders, peripheral neuropathies, neuromuscular junction diseases, and cerebrospinal diseases.
When ndings such as atrophy of the tongue and
fasciculation, which is a small spasm of the muscle surface, are observed, the dentist should
exclude temporomandibular joint disease and
dental disease and then refer the patient to a neurologist [43].
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In advanced cases of bulbar palsy, muscle
atrophy causes tongue movement disorder, so
tongue massage is recommended. In cases of
severe spasticity, the patient may have difculty
in opening the mouth due to increased muscle
tone; instruct rehabilitation that opens the mouth
wide consciously several times daily. If the
patient bites down hard on the teeth, the cheek or
tongue may be bitten. In such cases, a mouthpiece can be made to protect the cheek and tongue
[44].
As the symptoms of bulbar palsy progress, it
becomes difcult to bolus formation in the oral
cavity and feed them into the pharynx, resulting
in increased residual bolus of food in the pharynx
and a higher risk of aspiration. In patients with
advanced ALS, abnormalities in the neuromodulation of saliva secretion can lead to increased
saliva production at rest, resulting in severe sialorrhea and aspiration of saliva. In such cases, the
use of a low-pressure continuous aspirator for
saliva that mechanically aspirates saliva is effective [45].
Anticholinergics can decrease salivary secretion in patients with increased salivation, but are
contraindicated in patients with glaucoma or
prostatic hypertrophy. Application of scopolamine ointment to the parotid gland equivalent
and tricyclic antidepressants can decrease salivation in patients with depression or emotional
dysregulation [45, 46]. Since these drugs are
prescribed by physicians, dentists need to work
closely with them in providing oral care.
Although botulinum toxin is reported to be
effective for sialorrhea [45, 46], it is not covered
by health insurance in Japan and is contraindicated in ALS.Patients with ALS severity I or II
may receive intravenous edaravone [47]. When
renal excretion antimicrobial agents are administered from the dentist to such patients, caution
should be exercised because concomitant use
may exacerbate renal dysfunction.
In addition, impaired respiratory function
increases the risk of aspiration by reducing the
ability to cough adequately. Peak cough ow
(PCF) is a simple test to estimate the risk of aspiration, and cough assistance is required when the
PCF is below 270L/min, and noninvasive posi-
tive pressure ventilation (NPPV) is required
when the PCF is below 160L/min [45].
Thus, the degree of dependence on medical care
increases as ALS progresses. While sharing
information with specialists, occupational therapists, speech therapists, home visit nursing care
stations, and nursing care workers, visiting dentists, together with dental hygienists, need to support patients’ recuperation by providing dental
treatment focusing on oral care [45]. The dentist
plays a major role in preventing aspiration pneumonia by maintaining oral hygiene, giving
instructions on the form of meals, and providing
swallowing training [44].
References
1. American Psychiatric Association. Diagnostic and
statistical manual of mental disorders. Fifth Ed.
DSM-5. Arlington, TX: VA: American Psychiatric
Association; 2013.
2. Braak H, Braak E. Neuropathological staging of
Alzheimer-related changes. Acta Neuropathol.
1991;82(4):239–59.
3. Braak H, Del Tredici K, Rub U, etal. Staging of brain
pathology related to sporadic Parkinson’s disease.
Neurobiol Aging. 2003;24(2):197–211.
4. Research group on future projections of the elderly
population with dementia in Japan. Health and labor
science research Grant-in-aid for special research
on health, labour and welfare sciences. Research on
the future estimation of the elderly population with
dementia in Japan. 2015. (in Japanese).
5. The Japanese Society of Neurology (Supervised).
Guidelines for the Treatment of Dementia Diseases
Committee. Dementia Disease Diagnosis Guidelines
for Dementia Care 2017 (Ninchishou shikkan shinryou guideline). Tokyo; Igakushoin. 2017. p6–7; (in
Japanese).
6. MHLW Science research Grant Comprehensive
research project for dementia control: prevalence of
dementia in urban areas and response to functional
impairment of life in dementia: a comprehensive
research report for 2011–2012 (Toshibu niokeru ninchishou yuubyouritsu to ninchishou no seikatsukinoushougai heno taiou H23–24). 2013; (in Japanese).
7. The Japanese Society of Neurology. Committee
for "Guidelines for the Diagnosis and Treatment
of Dementia" Guidelines for the Diagnosis and
Treatment of Dementia 2017. (Ninchishou shikkan
shinryou guideline 2017). Tokyo; Igakushoin. 2017.
p19–22; (in Japanese).
8. The Japanese Society of Neurology. Committee
for "Guidelines for the Diagnosis and Treatment
16 Neurological Diseases
https://t.me/medicina_free
313
of Dementia" Guidelines for the Diagnosis and
Treatment of Dementia 2017. (Ninchishou shikkan
shinryou guideline 2017). Tokyo; Igaku Shoin. 2017.
p204–205; (in Japanese).
9. Goldberg LS, Altman KW. The role of gastrostomy
tube placement in advanced dementia with dysphagia:
a critical review. Clin Interv Aging. 2014;9:1733–9.
10. The Japanese Society of Neurology. Committee
for "Guidelines for the Diagnosis and Treatment
of Dementia" Guidelines for the Diagnosis and
Treatment of Dementia 2017. (Ninchishou shikkan
shinryou guideline 2017). Tokyo; Igaku Shoin. 2017.
p118–138; (in Japanese).
11. FDA Grants Accelerated Approval for Alzheimer’s
Drug. US Food and Drug Administration. https://
www.fda.gov/news- events/press- announcements/
fda- grants- accelerated- approval- alzheimers- drug.
Accessed 7 Jun 2021.
12. Aragón F, et al. Oral health in Alzheimer’s disease:
a multicenter case-control study. Clin Oral Investig.
2018;22:3061–70.
13. Tonsker PP, et al. Periodontal disease, tooth loss
and dementia: Is there a link? A systemic review.
Gerodontology. 2017;34:151–63.
14. Oue H, etal. Tooth loss induces memory impairment
and neuronal cell loss in APP transgenic mice. Behav
Brain Res. 2013;252:318–25.
15. The Japanese Academy of Clinical Periodontology.
HP: http://www.jacp.net/perio/effect/ (in Japanese).
16. Shintani T, et al. Serum antibody titer test against
Porphyromonas gingivalis infection (Kansenshou
nitaisuru kesseikoutaika kensa). Nichikokukenkaishi.
2018;10(1):39–43; (in Japanese).
17. Shankar GM, etal. Amyloid-beta protein dimers isolated directly from Alzheimer’s brains impair synaptic
plasticity and memory. Nat Med. 2008;14(8):837–42.
18. Engelhart MJ, etal. Inammatory proteins in plasma
and the risk of dementia: the Rotterdam study. Arch
Neurol. 2004;61(5):668–72.
19. Sparks SP, et al. Serum antibodies to periodontal
pathogens are a risk factor for Alzheimer’s disease.
Alzheimers Dement. 2013;8(3):196–203.
20. Poole S, etal. Determining the presence of periodontopathic virulence factors in short-term postmortem
Alzheimer’s disease brain tissue. J Alzheimers Dis.
2013;36(4):665–77.
21. Ishida N, etal. Periodontitis induced by bacterial infection exacerbates features of Alzheimer’s disease in
transgenic mice. NPJ Aging Mech Dis. 2017;3(5):15.
https://doi.org/10.1038/s41514- 017- 0015- x.
22. Kamer AR, etal. TNF-alpha and antibodies to periodontal bacteria discriminate between Alzheimer’s
disease patients and normal subjects. J Neuroimmunol.
2009;219:92–7.
23. Holmes C, et al. Systemic inammation and disease progression in Alzheimer disease. Neurology.
2009;73(10):768–74.
24. Dominy SS, et al. Porphyromonas gingivalis in
Alzheimer’s disease brains: evidence for disease causation and treatment with small-molecule inhibitors.
Sci Adv. 2019;5(1):eaau3333. https://doi.org/10.1126/
sciadv.aau3333.
25. Saji N, etal. Analysis of the relationship between the
gut microbiome and dementia:a cross-sectional study
conducted in Japan. Sci Rep. 2019;9(1):1008.
26. Michikawa S, etal. Dentistry and dementia (Shika to
ninchishou). Tokyo: Media; 2015; (in Japanese).
27. Fisher RS, etal. Operational classication of seizure
types by the international league against epilepsy:
position paper of the ILAE commission and terminology. Epilepsia. 2017;58(4):522–30.
28. Sheffer IE, etal. ILAE classication of the epilepsies:
position paper of the ILAE commission for classication and terminology. Epilepsia. 2017;58(4):512–21.
29. Japanese Society of Neurology, Committee for
Epilepsy Treatment Guidelines. Guidelines for the
treatment of epilepsy 2018, 1st Ed. Tokyo; Igakushoin;
2018, p15–16; (in Japanese).
30. Shirasu K, Furusato K. Oral surgery (kouku
gekagaku). 3rd ed. Tokyo: Ishiyakushuppan; 2011.
p.229–30; (in Japanese).
31. Casetta I, et al. Phenytoin-induced gingival overgrowth: a community-based cross-sectional
study in Ferrara, Italy. Neuroepidemiology.
1997;16(6):296–303.
32. Kato T.Study on the mechanism of collagen metabolism in phenytoin-induced gingival overgrowth.
(Fenitoin yuuhatsusei shiniku zoushokushou ni kansuru koragen taishakikou no kaiseki). Shiyakuryohou.
2008;27:86–91; (in Japanese).
33. Shinotsuka O. Epilepsy and dentistry for the disabled (Tenkan to shougaisha shika). Epilepsy.
2013;7(2):107–11; (in Japanese).
34. Sugiyama K.Hiyari-hatto: what to do in such a situation? First aid techniques during dental treatment
(Hiyari-hatto: Konnatoki Dousuru? Shikachiryou no
Kyukyu Technique). Tokyo: Nagamatsu shoten; 2005.
p.74–9; (in Japanese).
35. Seppi K, et al. Update on treatments for nonmotor
symptoms of parkinson’s disease—an evidence-based
medicine review. Mov Disord. 2019;34(2):180–98.
36. Seppi K, Ray Chaudhuri K, Coelho M, Fox SH,
Katzenschlager R, Perez Lloret S, Weintraub D,
Sampaio C.The collaborators of the Parkinson's disease update on non-motor symptoms study group on
behalf of the movement disorders society evidencebased medicine committee. Update on treatments
for nonmotor symptoms of Parkinson's disease an evidence-based medicine review. Mov Disord.
2019;34:180–98.
37. DeBowes SL, etal. Parkinson’s disease:considerations
for dental hygienists. Int J Dent Hyg. 2013;11:15–21.
38. Shirakawa M. Dental treatment for the sick
(Yubyoushashikashinryo). Tokyo: Ishiyaku shuppan;
2000. p.85–8; (in Japanese).
39. Nishida M.Illustrated guidelines for dental treatment
of the sick elderly. Tokyo: Quintessence Publishing;
2008. p.235–7; (in Japanese).
40. Japanese Society of Neurology. Guidelines for the
treatment of amyotrophic lateral sclerosis 2013;
314
https://t.me/medicina_free
M. Nishina et al.
https://www.neurology- jp.org/guidelinem/als2013_
index.html (in Japanese) https://www.neurology- jp.
org/guidelinem/als2013_index.html.
41. Japan ALS Association. Information on treatment research and clinical trials; http://alsjapan.
org/2019/06/15/post- 2398/. (in Japanese).
42. Ando T. Borderline areas amyotrophic lateral sclerosis misdiagnosed as spinal cord disease neurological
diseases that are prone to happen. (Kyoukai ryouiki
shitteokitai kinishukusei sokusakukoukashou sekitsuisekizuishikkan to goshin shiyasui shinkeinaikateki shikkan). Rinseigai. 2018;53(11):1020–2; (in Japanese).
43. Tomomatsu N, et al. A case of amyotrophic lateral sclerosis (ALS)associated with oral symptom
(Koukushoujou wo shusoni raiinshita ALS no 1 rei).
Nichiguchigaishi. 2014;60(3):142–6; (in Japanese).
44. Umemoto G. How to cooperate with dentistry—to
support the lives of the elderly—collaborative care
with dentistry for neuromuscular diseases (Shikatono
renkeiwo dousuru koureishano seikatsuwo sasaeruta-
meni. Shinkeikinshikkanno shinryou niokeru shikatono renkei). Prog Med. 2017;37(10):1157–61; (in
Japanese).
45. Ogino M. Amyotrophic lateral sclerosis.
Respiratory care for amyotrophic lateral sclerosis (Kinishukusei sokusakukoukashou.
Kinishukuseisokusakukoukashou no kokyukanri).
Jpn J Rehabil Med. 2018;55(7):545–50; (in Japanese).
46. Matsuda C, et al. Analysis of resting salivation rate
in patients with amyotrophic lateral sclerosis using
tracheostomy invasive ventilation (Kikansekkai kayouatsukanki dounyuugo no kinishukusei sokusakukoukashoukanjano anseiji daekibunpitsuryou). Clin
Nerve. 2016;56(7):465–71; (in Japanese).
47. Yoshino H. Subjects of regional alliances for amyotrophic lateral sclerosis~from the standpoint of neurology clinic (Kinishukuseisokusakukoukashou
no chiikirenkei no kadai. Shinkeinaika clinic no
tachibakara). Neurotherapy. 2017;34(3):273–4; (in
Japanese).
Neuropsychiatry Diseases
https://t.me/medicina_free
KotaroOtsuka, SeigoOhba, AsakiMatsuzaki,
TetsuakiArai, TadaharuKobayashi,
andNorifumiNakamura
17
1 Schizophrenia
KotaroOtsuka
1.1 Concept, Denition,
andPathophysiology
Schizophrenia is known as a disorder with a high
prevalence in adolescents. Schizophrenia is characterized by positive symptoms such as hallucinations, delusions, thought disorder, and disturbance
K. Otsuka
Department of Neuropsychiatry, Iwate Medical
University School of Medicine, Yahaba, Iwate, Japan
S. Ohba
Department of Regenerative Oral Surgery, Graduate
School of Biomedical Sciences, Nagasaki University,
Nagasaki, Japan
A. Matsuzaki · T. Arai (*)
Psychiatric Department, University of Tsukuba,
Tsukuba, Ibaraki, Japan
e-mail: 4632tetsu@md.tsukuba.ac.jp
T. Kobayashi
Division of Reconstructive Surgery for Oral and
Maxillofacial Region, Department of Tissue
Regeneration and Reconstruction, Niigata University
Graduate School of Medical and Dental Sciences,
Niigata, Japan
N. Nakamura
Kagoshima University, Kagoshima, Japan
Department of Oral and Maxillofacial Surgery,
Universitas Indonesia, Jakarta, Japan
of self-awareness, and negative symptoms such as
blunted affect, autism, social withdrawal, and
abulia and apathy. In the acute phase, positive
symptoms such as hallucinations and delusions
appear, and in the chronic phase, negative symptoms such as decreased motivation and blunted
affect, and social activities are affected depending
on the degree of neurocognitive dysfunction. The
diagnosis is made according to the ICD classication or the DSM classication of the American
Psychiatric Association. Many patients require
long-term, continuous pharmacotherapy. Patients
also receive a wide range of care, such as psychiatric rehabilitation and employment support,
while leading a social life.
1.2 Symptoms
1.2.1 Hallucinations
Hallucinations are often observed in schizophrenia, including verbal auditory hallucinations
(phantom voices) in which a person’s voice can be
heard, auditory hallucinations in which a person
speaks and responds, and visual hallucinations in
which a person’s thoughts can be heard as voices.
Sensory hallucinations are also often observed, in
which abnormalities in bodily sensations are experienced in the form of hallucinations. In addition,
tactile hallucination such as “touching the body,”
olfactory hallucination, gustatory hallucination,
visual hallucination are also sometimes observed.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
T. Chiba, H. Yamada (eds.), Internal Medicine for Dental Treatments,
https://doi.org/10.1007/978-981-99-3296-2_17
315
316
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K. Otsuka et al.
1.2.2 Delusion
Delusions are classied into primary delusions,
in which we intuitively have false beliefs, and
secondary delusions, which are based on other
experiences such as emotions and are understandable to some extent. Typical types of delusions include delusion of persecution, delusion of
reference, delusion of observation, delusion of
pursuit, and delusion of poisoning.
1.2.3 Disturbance ofSelf-Awareness
Self-consciousness disorder refers to a disturbance in the sense of self-identity, that is, the
sense that one’s thoughts and actions belong to
oneself. For example, in depersonalization, the
sense of reality is lost. In addition, the experience
of being made (artice experience) is an experience in which the self is inuenced and moved by
external forces, deprivation of thought, thought
insertion, thought propagation, mind reading are
recognized.
1.2.4 Obstacles toThought Path
Disorders of the thought process are often present, including loosening association, incoherent
thinking, blocking of thought.
1.2.5 Abnormalities ofMood
In the acute phase, anxiety, emotional instability,
and excitement are also observed, but often there
is blunting of emotions and attening of emotions, which is a state of diminished emotional
response to external stimuli. In addition, sometimes the depression may increase when the
symptoms are alleviated, and it is necessary to
pay attention to the post-schizophrenic depression and the risk of suicide.
1.2.6 Impairment ofMotivation
Disorders of motivation may include the following symptoms: stupor, catatonic stupor, abulia,
rejection, and stereotypy.
1.2.7 Neurocognitive Dysfunction
In schizophrenia, neurocognitive dysfunction in
various domains is observed, including impaired
attention, processing speed and uency, problemsolving ability, memory, and working memory.
1.3 Treatment
The goals of care for schizophrenia (WHO) are (1)
to identify the illness as soon as possible; (2) to treat
the symptoms; (3) to provide the patient and family
with skills; (4) to maintain improvement over time;
(5) to prevent relapse; and (6) to reintegrate the
patient into the community so that he or she can
lead a normal life [1]. In order to achieve these
goals, the following are important in treatment: (a)
pharmacotherapy to control symptoms and prevent
recurrence; (b) education and psychosocial interventions to help patients and their families cope
with the disease and its complications and to prevent recurrence; and (c) rehabilitation to reintegrate
patients into the community and to help them reacquire educational and vocational functions [1].
Psychosocial treatments include psychotherapy, which focuses on the patient’s problems
while building a trusting relationship with the
patient, compliance with medication, and life
concerns; psychoeducation, which promotes
understanding of the disease; social skill training
(SST), which is based on learning social skills;
and occupational therapy (OT), which focuses on
occupational activities.
Pharmacotherapy is the most important part of
treatment. The risk of relapse in rst-episode
schizophrenic patients with medication interruption
is very high, 4.89 times, and 4.57 times for secondepisode schizophrenic patients [2], it is important to
continue pharmacotherapy. Delay in treatment
causes a number of disadvantages, such as delayed
recovery, poorer prognosis, reduced psychosocial
skills, loss of family and social support, increased
suicide risk, and higher health care costs [3].
The mainstay of pharmacotherapy is antipsychotic medication, which includes standard and
second-generation (atypical) antipsychotics.
Standard antipsychotics, introduced 50 years
ago, help to reduce or eliminate symptoms of
schizophrenia, such as thought disorder, hallucinations and delusions, and reduce associated
symptoms, such as excitement, impulsiveness,
and aggression, such as chlorpromazine (1955),
levomepromazine (1960) and haloperidol (1964).
The side effects of long-term treatment with typical antipsychotics are listed in Table17.1.
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