BLOCK 4.

1
DISTURBANCES in
RESPIRATORY DRIVENEUROLOGIC DISEASE
ASTUTI
NEUROLOGIST
SLEEP SUBDIVISION, NEUROLOGY DEPT. GMU
SLEEP CLINIC SARDJITO HOSPITAL

Kasus 1
Tn X, 58 th dirawat di unit stroke
dengan :
- Penurunan kesadaran, ec. Stroke
infark,
- hipertensi, T: 160/100,

Breathing ?

Kasus 2
Laki laki 65 tahun dengan keluhan insomnia
Setiap bangun tidur, os mengeluh badan
lesu tidak segar, kurang konsentrasi, mudah
tersinggung, pelupa.
Riwayat hipertensi dan penyakit jantung
(+)
Os ke klinik gangguan tidur untuk menjalani
PSG (Poly Somnography) --- tayangan
video.

Tayangan video : 1, 2, 3,

Breathing is an active process generated

and modulated in the respiratory system
and
nervous system subject to a
complex set of neural systems located
mainly in brainstem.

patomekanisme
Breathing is altered in many neurologic
diseases due to several
mechanisms:
1.lesions of the areas that control
breathing,
2.lesions or diseases that produce apnea,
paralysis or poor breathing (caused by
neuromotor disease) or treatments
given to control neurologic symptoms.

The Central Respiratory Motor

It has been knownMechanisms
for more than a century that breathing

is controlled mainly by the lower brainstem,and that

each half of the brainstem is capable of producing an
independent respiratory rhythm. In patients with
poliomyelitis, for example, the occurrence of respiratory
failure was associated with lesions in the ventrolateral
tegmentum of the medulla (Feldmen, Cohen). Until
recently thinking on this subject was dominated by
Lumsdens scheme of the breathing patterns that
resulted from sectioning the brainstem of cats at various
levels. He postulated the existence of several centers in
the pontine tegmentum, each corresponding to an
abnormal breathing pattern-a pneumotaxic center, an
apneustic center, and a medullary gasping center.

 Three paired groups of respiratory nuclei are

oriented more or less in columns in the pontine
and medullary tegmentum (Fig. 26-7). They
comprise (1) a ventral respiratory group (referred
to as VRG), extending from the lower to the upper
ventral medulla, in the region of the nucleus
retroambiguus; (2) a dorsal medullary respiratory
group (DRG), located dorsal to the obex and
immediately ventromedial to the nucleus of the
tractus solitaries (NTS); and (3) two clusters of
cells in the dorsolateral pons in the region of the
parabrachial nucleus. From electrical stimulation
experiments, it appears that paired neurons in the
dorsal pons may act as on-off switches in the
transition between inspiration and expiration.

Voluntary Control of
Breathing

During
speech,
swallowing,
breath-holding,
or
voluntary
hyperventilation, the automaticity of
the
brainstem
machanisms
of
respiration is arrested in favor of
reflexive or of conscious control of
diaphragmatic contraction.

Afferent Respiratory
Influences

A number of signals that modulate

respiratory
drive
originate
in
chemoreceptors
located
in
the
carotid artery. These receptors are
influenced both by changes in pH and
by hypoxia. Chemoreceptor afferents
pass along the carotid sinus nerves,
which join the glossopharyngeal
nerves and terminate in the NTS.

Ax
PX fisik
Px Neurologis
Assess breathing

Assessment

sign & Symptom

pathologic lesion at various levels of the brain.
breathing spontaneously
rate of breathing
pattern of breathing
The respiratory pattern is helpful in localizing and, in
certain
instances, determining the nature of the process.
Berbagai macam pola nafas bisa memberi arti lokasi lesi pada
pasien dengan perubahan kesadaran.
Pola-pola ini bisa diketahui dari observasi langsung di tempat
tidur.

Miastenia gravis (apnea)

Guillan Bahre Syndrome
Metabolik
CHF (Congestive Heart Failure)
cheyne stokes
Deep coma (Central Reflex
Hyperventilation)
Obat obatan (depressed breathing)

CONT.
Moreover, respiratory failure is one of
the most disastrous disturbances of
neurologic function in comatose
states and in neuromuscular diseases
such as myasthenia gravis, GuillainBarre syndrome, amyotrophic lateral
sclerosis, muscular dystrophy, and
poliomyelitis.

etiologi

Metabolic acidosis (e.g., diabetic

ketoacidosis, uremia, ingestion of
organic acids, lactic acidosis)
Respiratory alkalosis (e.g., hepatic
encephalopathy, salicylate poisoning)

Coma with hyperventilation

etiologi
Hyperventilation,
central
apnea
attacks, nocturnal stridor, sleep
breathing
disorder
(SBD)
are
breathing
problems
that
are
increasingly recognized as common
features
of
several
neurologic
disorders.

Neuromuscular Respiratory
Failure in Critically III Patients
Caused by the acute neurmuscular
acritical illness palyneuropathy, a
critical illness myopathy generalized
weakness and respiratory failure

obstructive sleep apnea syndrome (OSAS) is one

of the most common sleep problems, with
prevalence of more than 24% of the adult
population.
OSAS and other SBD occur even more often with
prevalence in patients with neurologic diseases like
:
- stroke,
- dementia,
- Parkinsons disease (PD)
- atypical Parkinsonian syndromes
- myelopathies,
- motor neuron diseases
- polyneuropathy,
- diseases related to the motor end-plate
- myopathies,

The congenital central

hypoventilation syndrome
is Neurologic lesions that cause
hyperventilation are diverse and
widely located throughout the brain.
The traditional view of central
neurogenic hyperventilation as a
manifestation of a pontine lesion.

Diagnosis
Klinis /tipe ?
Topik / Letak lesi ?
Etiologi ?

BREATHING DISORDERS
TYPE
Cheyne-Stokes respiration
Central neurogenic
hyperventilation
Apneustic breathing
Ataxic breathing
Depressed breathing
Coma with hyperventilation

Cheyne-Stoke respiration

Central Neurogenic Hyperventila

Apneusis

Cluster Breathing
Ataxic Breathing

Abnormal Breathing Patterns

Cheyne-Stokes
crescendo/decrescendo pattern mixed with
apnea
bilateral hemisphere dysfunction
Central neurogenic hyperventilation
rapid deep breathing
lesion between midbrain and pons
Apneustic breathing
prolonged inspiration followed by apnea
pontine dysfunction
Ataxic breathing
irregular pattern
medullary dysfunction-close to death
Coma with hyperventilation
metabolic derangement
Coma with hypoventilation
drug overdose
COPD

ABNORMAL RESPIRATORY PATTERNS

(ABNORMAL SHADED AREA) (Plum
1980)
Cheyne-Stoke respiration
a. Cheyne-Stokes respiration:
massive tentorial lesion, bilateral
deep-seated cerebral lesions or
metabolic disturbances of the
brain,
failure.
Centralcongestive
Neurogenic heart
Hyperventilation
b. Central neurogenic
hyperventilation: lower midbrainApneusis
upper
pontine tegmentum, either
primary or secondary to a
tentorial herniation
Clusterlow
Breathing
c. Apneustic breathing:
pontine
lesion, usually due to basilar
artery occlusion.
Ataxic Breathing
d. Cluster breathing: high medullary
damage

Cheyne-Stokes respiration
Cheyne- Strokes breathing indicates
bilateral deep hemispheric and basal
ganglionic dysfunetion. The upper
brainstem also may be involved.
Note : Cheyne-Strokes respiration is
most commonly observed in non
neurologic
conditions,
such
as
congestive heart failure.

Cheyne-Stokes breathing
the common and well-known waxing and
warning type of cyclic ventilation reported by
cheyne in 1818 and later elaborated by
Stokes, has for decades been ascribed to a
prolongation of circulation time, as in
congestive heart failure; but there are data
that support a primary neural origin of
disorder, particularly the observation that it
occurs most often in patients with deep
hemisphere
lesions
of
the
cerebral
hemispheres.

Central neurogenic
hyperventilation
refers to continuous rapid, regular, and deep
respirations at a rate of about 25/minute.
correlates with increasing depth of coma.
Systemic acidosis (e.g., diabetic keto
acidosis,
lactic
acidosis)
and
hypoxemia should be excluded (two
partial
pressure
of
oxygen
[PO2]
determinations over 70 mm Hg in 24 hours
in considered adequate for this purpose)
before it is concluded that hyperventilation
is of neurogenic origin.

Apneustic breathing
consists of a prolonged inspiratory
phase followed by apnea (the
inspiratory cramp). Either pattern
implies pontine damage.

 Ataxic breathing and gasping

breathing (Biots respirations) imply
damage to the medullary respiratory
centers.
Depressed breathing consists of
shallow, slow, and ineffective breathing
caused by medullary depression,
usually produced by drugs.

Dyspnea
The
common
respirotary
sensations
of
breathlessness, air hunger, chest tighness, or
shortness of breath, all subsumed under the term
dyspnea,
have
defied
neuropsysiologic
interpretation.
Neurons in the thalamus and central midbrain
tegmentum fire in a graduated manner as
respiratory drive is increased. These neurons are
influenced greatly by afferent information from the
chest wall, lung, and chemoreceptors and are
postulated to be the thalamic representation of
sensation from the thorax that is perceived at
cortical level as dypsnea.

Aberrant Respiratory
Patterns
Many of most interesting respiratory
patterns observed in neurologic disease
are found in comatose patients, and
several of this patterns have been
assigned localizing value, some of
certain validity : central neurogenic
hyperventilation, apneusis and ataxic
breathing. These are discussed in
relation to the clinical signs of coma

Another striking aberration of

ventilation
is a loss of automatic respiration
during sleep, with preserved
voluntary breathing (On-dines
curse)

Therapy
The major part of the treatment of
these disorders consists of measures
- Position
- Oxygenation
- assist respiration
(mechanical ventilators).

Fixed pressure CPAP/auto-adjusted CPAP is

The most effective treatment of OSAS.
This probably also includes patients with
OSAS and neurologic diseases.
Bi-level PAP/variable PAP, NIPPV and
volumetric ventilation is useful for
- SBD-like central apneas,
- Cheyne-Stokes breathing,
- alveolar hypoventilation.

Prognosis
Finally, death-or brain death-is now
virtually defined in trems of the
ability of the nervous system to
sustasin respiration, a reversion to
ancient methods of determining the
cessation of all vital forces.

Reference :
Samuel, M. A., 2005. Manual of
Neurologic Therapeutics, 7th Edition,
Little, Brown and Company, Boston.
Ropper, A.H. & Brown, R.H., 2007.
Adams and Victor`s PRINCIPLES OF
NEUROLOGY. McGraw-Hill
Companies,Inc. USA.

SLEEP RELATED BREATHING

DISEASE
CENTRAL SLEEP APNEA SYNDROME
1. Primary Central Sleep Apnea
2. Central Sleep Apnea due to Cheyne
Stokes Breathing Pattern
3. CSA due to Medical Condition not
Cheyne Stokes
4. CSA due to High Altitude Periodic
Breathing
5. CSA due to drug or Substance

Sleep Apnea

Pauses in breathing due

to obstruction in airway
causing gasps and
arousals during sleep
18 million affected
--mostly males
Risk Factors: Obesity
and/or have high blood
pressure, persons with
upper airway physical
abnormality
Lowers blood-oxygen
levels & increases work of
heart
Associated with
cardiovascular

Sleep apnea
Ventilasi dikendalikan 3 proses:
-automatic/metabolik kontrol system
- behavioral system
- wakefullness stimulus

Sleep Apnea: Two Types

Obstructive Sleep Apnea: most
common
Central Sleep Apnea

Obstructive Sleep Apnea

Classic- obese, middle-aged male
with thick neck or enlarged tonsils
Apneas- brief gaspssilence,
followed by loud resuscitative
snores, and sometimes body
movements (restless)
Usually unaware of snoring,
arousalsbut sleep partner is aware

Central Sleep Apnea

Apneas- episodic cessation of central
ventilation drive
Thus snoring is less common

More in elderly, with underlying CNS

lesions- ex. tumor, stroke

Respiratory polygraphy
has a moderate sensitivity and specificity in the
diagnosis of OSAS without neurologic diseases
Its value for diagnosis of other SBD or in patients with
OSAS with neurologic diseases has not been
evaluated compared to gold standard PSG.
Limited channel polygraphy oximetry has a poor to
moderate sensitivity-specificity for the identification
of OSAS in patients without neurologic diseases.
Oximetry
- cannot differentiate between obstructive and
central
sleep apnea or is insufficient to identify stridor.
- has a role for the screening of hypoventilation in
patients with neuromuscular weakness.
Furthermore,
- useful for the control of CPAP treatment.

Sleep Apnea: Consequences

Depression
Anxiety
Morning headaches
Cognitive dysfunction
Hypertension