Добавил:

fench Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Сумский государственный университет

Предмет:

Нормальная анатомия

Файл:

Color Atlas of Neurology

.pdf

Скачиваний:

201

Добавлен:

11.08.2013

Размер:

18.87 Mб

Скачать

☆

<<< < Предыдущая 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 3839 / 4539 40 41 42 43 44 45 > Следующая >>>

Appendix

Table 23 Causes of chronic daily headache (p. 182)

Type of Headache	Symptoms and Signs/Syndromes

Primary headache
Chronic tension	See p. 182
headache
Migraine	Mild to severe, often unilateral pain (transformed migraine). Additional migraine at-
	tacks (p. 184)
Atypical facial pain	Unilateral or bilateral pain, often predominantly felt in the nasolabial or palatal region,
	often very severe. Unresponsive to a wide variety of medical and surgical therapies.
	Normal findings on a wide variety of diagnostic tests (“diagnosis of exclusion”)
Secondary headache	Posttraumatic, drug-induced, vascular (p. 182), intracranial mass, hydrocephalus, sinusi-
	tis, parkinsonism, cervical dystonia, myoarthropathy of the masticatory apparatus,1
	mental illness (depression, schizophrenia, hypochondria), cervical spine lesions
	(degenerative lesions, fractures, Klippel–Feil syndrome), Down syndrome, basilar im-
	pression, osteoporosis, skull metastasis, spondylitis, rheumatoid arthritis, lesions of cer-
	vical spinal cord/meningismus (tumor, hemorrhage, syringomyelia, cervical myelopathy,
	von Hippel–Lindau syndrome, meningitis, carcinomatous meningitis, intracranial hypo-
	tension)

1 Temporomandibular joint dysfunction, oromandibular dysfunction.

Table 24 Prognostic factors in epilepsy (p. 198)

Favorable Prognostic Factors	Unfavorable Prognostic Factors

One seizure type	Multiple seizure types
No interictal neurological deficit	Interictal neurological deficit
Older age of onset	Younger age of onset
Seizures secondary to a treatable disease	Spontaneous seizures
Individual seizures of short duration	Status epilepticus
Frequent seizures	Infrequent seizures
Good response to anticonvulsants	Poor response to anticonvulsants
	(Neville, 1997)

Appendix

373

Appendix

374

Appendix

Table 25 Causes of syncope (p. 200)

Cause	Underlying Condition/Trigger

Cardiac	Arrhythmia (bradyrhythmia, tachyrhythmia, or reflex arrhythmia), heart disease (e. g.,
	cardiomyopathy, myxoma, mitral stenosis, congenital malformation, pulmonary em-
	bolism)
Hemodynamic	Hypovolemia, hypotension (vasovagal as an emotional reaction to pain, anxiety, sudden
	shock, sight of blood; hypotension from prolonged standing, heat, exhaustion, alcohol;
	multiple system atrophy; polyneuropathies, e. g., amyloid, hereditary, toxic; polyradicu-
	lar neuropathies/Guillain–Barré syndrome; antihypertensive agents, nitrates, other
	drugs; postural orthostatic tachycardia syndrome = POTS; paraplegia above T6)
Cerebrovascular	Subclavian steal syndrome, basilar migraine, Takayasu disease
Metabolic	Hypoglycemia, hyperventilation, anemia, anoxia, postprandial (older individuals)
Miscellaneous	Coughing fit (cough syncope = tussive syncope = laryngeal syncope), micturition (mic-
	turition syncope), defecation, prolonged laughing (“laughing fit”, geloplegia), glos-
	sopharyngeal neuralgia, affect-induced respiratory convulsion in childhood (breath-
	holding spells), pop concerts (teenage females), lying in supine position during preg-
	nancy (supine syndrome)
	(Bruni, 1996; Lempert, 1997)

Table 26 Causes of sudden falling without loss of consciousness (p. 204)

Type of Fall/Pathogenesis	Cause	Features

Drop attack	TIA1 in vertebrobasilar territory	Usually accompanied by dizziness,
		diplopia, ataxia, or paresthesias
	TIA in anterior cerebral artery	Seen when the two anterior cere-
	territory	bral arteries arise from a common
		trunk
	Colloid cyst of 3rd ventricle	Position-dependent headache
	Posterior fossa tumor	Sudden fall after flexion of neck
Parkinsonism	Parkinson disease, multiple	See p. 206 f
	system atrophy
Muscle weakness	Myopathy, Guillain–Barré syn-	See p. 50 f
	drome, polyneuropathy, spinal
	lesions
Spinal or cerebellar ataxia, gait	Funicular myelosis, cerebellar	See specific diseases
apraxia	lesions, metabolic encephalo-
	pathies, hydrocephalus, lacunar
	state, cervical myelopathy, multi-
	ple sclerosis
Cryptogenic	Unknown	Occurs in women over 40 while
		walking
Vestibular disorder	Ménière disease (vestibular drop	Dizziness, nausea, nystagmus, tin-
	attack Tumarkin otolithic crisis);	nitus. Vestibular drop attacks may
	occasionally due to otitis media,	occur in isolation
	toxic or traumatic causes
Cataplexy	Loss of muscle tone triggered by	Alone or with narcolepsy
	emotional stimuli (fright, laughter,
	anger)
1 Transient ischemic attack.

	Appendix

Table 27 Diagnostic criteria for multiple sclerosis (pp. 216, 218)

Manifestations	Additional Information Needed for Diagnosis

Two or more episodes; objective eviden-	None
ce1 of 2 or more lesions
Two or more episodes; objective evidence	Disseminated lesions (MRI2) or two or more MS-typical lesions
of 1 lesion	(MRI and positive CSF tests3) or relapse4
One episode; objective evidence of 2 or	Dissemination of lesions over time (MRI5) or relapse
more lesions
One episode; objective evidence of 1 le-	Disseminated lesions (MRI2) or two or more MS-typical lesions
sion (monosymptomatic syndrome)	(MRI + positive CSF findings3) + dissemination of lesions over
	time (MRI5) or relapse
Gradual worsening of neurological	Positive CSF findings3 + disseminated lesions6 or pathological
manifestations suggestive of MS	VEP + 4–8 cerebral lesions7 + dissemination of lesions over time
	(MRI5) or continuous progression for 1 year

(McDonald et al., 2001)

1 MRI, CSF, visual evoked potentials (VEP). 2 For special criteria, see McDonald et al., 2001. 3 Oligoclonal immunoglobulin, elevated IgG index. 4 Topographic-anatomic classification differs from that of previous episodes. 5 Follow-up examination after an interval of at least 3 months; for special criteria, see McDonald et al., 2001. 6 Nine or more cerebral lesions or two or more spinal lesions or 4–8 cerebral lesions + 1 spinal lesion. 7 In patients with fewer than 4 cerebral lesions, at least 1 additional spinal lesion must be observed by MRI.

Table 28 Therapeutic guidelines for meningoencephalitis (p. 224)

Clinical Features	Additional Findings	Treatment1

Previously healthy patient	Gram-positive cocci in CSF	Vancomycin + cephalosporin
	Gram-negative cocci in CSF	Penicillin G
	Gram-positive bacilli in CSF	Ampicillin or penicillin G +
		aminoglycoside3
	Gram-negative bacilli in CSF	Cephalosporin2 + aminoglycoside3
Previously healthy patient	Negative CSF Gram stain5	Bacterial infection suspected:
		cephalosporin2. Age !50 years +
		ampicillin
		Viral infection suspected: influenza
		A, amantadine or rimantadine;
		herpes simplex (p. 236); cytome-
		galovirus (p. 244); poliovirus
		(p. 242); HIV (p. 241); varicella
		zoster (p. 239)
Septic focus (e. g., mastoiditis),	Supportive evidence from imaging	Vancomycin + cephalosporin2
neurosurgery, head trauma	study, e. g., CT with bone windows
Immune deficiency/immunosup-	(possible) Brain stem signs, Gram-	Ampicillin + ceftazidime
pressant therapy4	negative bacilli in CSF
Nosocomial infection	(possible) Gram-negative bacilli in	Cephalosporin2 + e. g., oxacillin or
	CSF	fosfomycin + aminoglycoside3
Focal neurological signs	Temporal lobe process demon-	Acyclovir (p. 236)
	strated by EEG, CT and/or MRI
Spinal and radicular pain	Spinal epidural abscess confirmed	Cephalosporin2 + (e. g.) oxacillin
	by imaging study (MRI, myelogra-	or fosfomycin + aminoglycoside3.
	phy, or CT)	Surgery
Neonate ("3 months of age)	Negative CSF Gram stain	Ampicillin + cephalosporin2

1 Drugs recommended by Quagliarello and Scheld (1997). 2 E.g., cefotaxime or ceftriaxone. 3 Gentamycin or tobramycin. 4 Predisposes to tubercular, fungal, and other opportunistic infections (pp. 233, 245 f). 5 Aseptic/viral meningitis, p. 234.

Appendix

375

Appendix

Table 29 Bacteria commonly causing meningitis and meningoencephalitis (p. 226)

Pathogen	Portal of Entry/Focus	Clinical Features

Pneumococcus (S. pneumoniae/	Nasal and pharyngeal mucosa,	Meningitis may be accompanied or
Gram+ extracellular diplococ-	head trauma, neurosurgical	preceded by sinusitis, otitis media or
cus) adults1	procedures, external CSF	pneumonia. Posttraumatic meningitis
	drainage	may occur several years after trauma; re-
		current meningitis (CSF leak? Im-
		munodeficiency?). Course may be hyper-
		acute (nonpurulent meningitis2), acute or
		subacute (days to weeks). Epileptic
		seizures. Risk of brain abscess, subdural
		empyema or cerebral vasculitis
Meningococcus (N. meningitid-	Nasopharynx	Hyperacute course with sepsis,
is3/Gram– intracellular diplo-		adrenocortical insufficiency and consump-
coccus) children and ado-		tion coagulopathy (Waterhouse–Frider-
lescents4		ichsen syndrome). Petechial or confluent
		cutaneous hemorrhages. Myocarditis/peri-
		carditis
Haemophilus influenzae (Gram–	Nasal and pharyngeal mucosa	Usually type B. May be accompanied or
bacillus) children and ado-		preceded by sinusitis, otitis media, or
lescents		pneumonia
Listeria (L. monocytogenes/	Gastrointestinal tract (con-	Focal neurological deficits, particularly
Gram+/organism difficult to	taminated food, e. g., dairy	brain stem encephalitis (rhombencephali-
identify) neonates5, adults	products or salads)	tis), are commonly seen.
!50 years of age		Predisposing factors: pregnancy, old age,
		alcoholism, immune suppression, primary
		malignancy. CSF findings are extremely
		variable (“mixed cell picture”)
Staphylococcus (S. aureus/	Endocarditis, head trauma, ex-	In association with sepsis, i. v. drug use,
Gram+) neonates and adults	ternal CSF drainage, lumbar	alcoholism, diabetes mellitus, primary
Enterobacter (Gram–/bacilli)	puncture, urinary tract,	malignancy
neonates	spondylodiskitis
M. tuberculosis (acid-fast bacil-	Extracerebral organ tuberculo-	See p. 232
lus)	sis

Gram+ = Gram-positive; Gram– = Gram-negative.

1 Age !18 years. 2 Very rapidly progressive meningitis, low cell count and high total protein and lactate levels in CSF, and CSF smear culture containing large quantities of bacteria. 3 Group A, Central Africa, South America; Group B, Europe; Group C, North America; type may change. 4 Age 3 months to 18 years. 5 Age "3 months.

Table 30 Viruses causing CNS infection (p. 234)

		Common	Occasional	Rare

		Meningitis
		Enteroviruses1,3, arboviruses2,3,	HSV type 14, LCMV3, mumps	Adenoviruses4, CMV4, Epstein–Barr virus
		HIV5, HSV type 24	virus3	(EBV)4, influenza virus A+B3, measles
				virus3, parainfluenza virus3, rubella virus3,
				varicella-zoster virus (VZV)4
		Encephalitis, myelitis
		Arboviruses, enteroviruses,	CMV, EBV, HIV, measles virus3,	Adenoviruses, influenza A, LCMV, parain-
		HSV type 1, mumps virus	VZV	fluenza virus, rabies virus3, rubella virus,
				HTLV-I5,6
376	1	Poliovirus 1–3, coxsackievirus (B5, A9, B3, B4, B1, B6), echovirus (7, 9, 11 30, 4, 6, 18, 2, 3, 12, 22), enterovirus
	1

(70, 71). 2 Arthropod-borne viruses, including alphaviruses, flaviviruses, pestiviruses, bunyaviruses, and orbiviruses. 3 RNA virus. 4 DNA virus. 5 Retrovirus. 6 Human T-cell lymphotropic virus type I causes myelitis.

					Appendix

Table 31 Grades of malignancy of brain tumors (p. 264)

Tumor		Grade I	Grade II	Grade III	Grade IV
		(benign)	(semi-	(malig-	(malig-
			benign)	nant)	nant)

Neuroepithelial tumors
Astrocytoma
! Fibrillary, protoplasmic, gemistocytic astrocytoma			+++	++
!	Anaplastic astrocytoma			+++
!	Glioblastoma ( = glioblastoma multiforme)				+++
!	Pilocytic astrocytoma	+++		+
!	Pleomorphic xanthoastrocytoma		+++	++
Oligodendroglioma
!	Oligodendroglioma		+++
!	Anaplastic oligodendroglioma			+++
Ependymoma
! Ependymoma (cellular, papillary, epithelial)		++	+++	++
!	Anaplastic ependymoma			+++
Mixed glioma
!	Oligoastrocytoma		+++
!	Anaplastic oligoastrocytoma			+++
Choroid plexus tumors
!	Plexus papilloma	+++
!	Plexus carcinoma			+++	++
Neuronal/mixed neuronal-glial tumors
!	Gangliocytoma	+++
!	Ganglioglioma		+++
!	Anaplastic ganglioglioma			+++
Pineal tumors
!	Pineocytoma	+++	++
!	Pineoblastoma (PNET)				+++
Embryonal tumors
! Primitive neuroectodermal tumor (PNET), see p. 260					+++
!	Neuroblastoma				+++
Cranial nerve tumors
!	Schwannoma	+++
Meningeal tumors
!	Meningioma	+++
!	Anaplastic meningioma			+++
Blood vessel tumors
!	Hemangiopericytoma		+++	++
!	Glomus tumor	+++
Lymphoma
!	Primary CNS lymphoma			++	+++
Germ cell tumors
!	Germinoma			+++
Intraand suprasellar tumors
!	Pituitary adenoma	+++		+
!	Craniopharyngioma	+++
Metastatic tumors					+++
		(Kleihues et al., 1993 and Krauseneck, 1997)

+++, Common; ++, Rare; +, Very rare.

Appendix

377

Appendix

Table 32 Karnofsky performance scale for quantification of disability (p. 264)

General Condition	%	Comments

Patient can perform normal daily activities and	100	Normal; no complaints; no evidence of disease
work without impairment
No specific treatment required	90	Able to carry on normal activity; minor impair-
		ment
	80	Normal activity with effort; some impairment is
		clearly evident
Patient cannot work; can meet most personal	70	Cares for self; cannot perform normal activities
needs, but needs some degree of assistance; can		or work
be cared for at home	60	Needs occasional assistance, but can meet most
	60	Needs occasional assistance, but can meet most
		personal needs
	50	Needs considerable assistance and frequent
		medical care
Patient cannot care for self; needs to be cared for	40	Disabled; requires special care and assistance;
in a hospital, nursing home, or at home by a		home nursing care still possible
nurse/family members. Disease may progress
rapidly	30	Severely disabled; hospitalization indicated al-
	30	Severely disabled; hospitalization indicated al-
		though death not imminent
	20	Gravely ill; hospitalization necessary
	10	Moribund

Table 33 Glasgow coma scale (p. 266)

I		II		III
Eye Opening	Score	Best Verbal Response	Score	Best Motor Response (arms)	Score

				Obeys commands	6
		Oriented	5	Selectively avoids painful stimuli	5
Spontaneous	4	Confused	4	Withdraws limb from painful	4
				stimuli
To speech	3	Single words	3	Flexes limb in response to painful	3
				stimuli
To pain	2	Meaningless utterances	2	Extends limb in response to pain-	2
				ful stimuli
No response	1	No response	1	No response	1
				(Teasdale, 1995)

The scores in columns I, II, and III are summed to yield the overall value.

GCS 13–15 = mild head trauma; GCS 9–12 = moderate head trauma; GCS 3–8 = severe head trauma.

378

Appendix

Table 34 Criteria for assessment of head trauma (p. 266)

Severity (GCS)1	Risk of	Symptoms and Signs 3
	Secondary
	Injury2

Mild (13–15)	Low	Impairment of consciousness lasting !1 hour
		Asymptomatic (or, at most: headache, dizziness, bruises, and lacera-
		tions)
Moderate (9–12)	Moderate	Impairment of consciousness at time of accident or thereafter, last-
		ing between 1 and 24 hours
		Increasingly severe headache
		Alcohol/drug intoxication
		No reliable description of accident. Multiple trauma, severe facial injur-
		ies, basilar skull fracture, suspicion of depressed skull fracture or open
		head injury. Posttraumatic epileptic seizure, vomiting, amnesia
		Age !2 years (except in minor accidents), possibility of child abuse
Severe (3–8)	High	Impairment of consciousness lasting !24 hours + brain stem syn-
		drome or
		Impairment of consciousness lasting "24 hours or
		Posttraumatic psychosis lasting "24 hours
		Impairment of consciousness not due to alcohol/substance abuse/medi-
		cations, and not a postictal or metabolic phenomenon
		Focal neurological signs
		Depressed skull fracture, open head injury

(White and Likavec, 1992) 1 Glasgow Coma Scale. 2 Patients with one or more manifestations from the list at right belong to the corresponding risk group. 3 Criteria for assessment of severity are in bold type.

Table 35 Late complications of head trauma (p. 268)

Complications	Clinical Features	Remarks

Posttraumatic syn-	Headache, nausea, vertigo, orthostatic	Usually follows mild head trauma; may
drome	hypotension, depressed mood, irritability,	cause significant psychosocial impairment
	fatigue, insomnia, impaired concentration
Chronic subdural	Headache, behavioral change, focal signs	Usually follows mild trauma (predisposing
hematoma (SDH)		factors: old age, brain atrophy, alco-
		holism)
Subdural hygroma	Same as in chronic SDH	Symptoms may improve when the patient
		is lying down and worsen on standing
CSF leak	Drainage of CSF from the nose or ear; risk	CSF rhinorrhea worsens on head flexion.
	of recurrent meningitis, brain abscess	CSF otorrhea indicates a laterobasal skull
		fracture
Hydrocephalus	Headache, behavioral change, urinary in-	Normal pressure hydrocephalus, venous
	continence	sinus thrombosis
Epilepsy	Focal/generalized seizures	May arise years after head trauma
Encephalopathy	Behavioral changes	See p. 122ff. Types include septic en-
		cephalopathy, punch-drunk en-
		cephalopathy (p. 302, Table 44)
Critical illness neu-	Prolonged ventilator dependence, weak-	Associated with sepsis and multiple organ
ropathy and my-	ness	failure
opathy
Heterotopic ossifi-	Restricted mobility of joints, pain	Due to muscle trauma
cation (myositis
ossificans)
Complications of	Bed sores, peripheral nerve lesion, joint	Ensure proper positioning and frequent
immobility	malposition	changes of position (especially of para-
		lyzed limbs)

Appendix

379

Appendix

380

Appendix

Table 36 Spinal fractures (p. 272)

Fracture/Dislocation		Pathogenesis		Stability1

Cervical spine
!	Atlantoaxial dislocation	! Dislocation between C1 and C2		!	Unstable
!	Jefferson’s fracture2	!	Axial trauma	!	Unstable
!	Dens fracture	!	Hyperflexion	!	Unstable3
! Bilateral axis arch fracture4		!	Hyperflexion and distraction	!	Unstable
! Dislocation fracture of C3–7		!	Hyperflexion	!	Unstable
!	Lateral compression fracture	!	Flexion and axial compression	!	Stable
Thoracic spine, lumbar spine
!	Compression fracture	Fall (back, buttocks, extended legs),		!	Stable
		direct trauma. These fractures may be
		pathological (osteoporosis, myeloma,
!	Burst fracture	metastasis)		!	Stable
!	Burst fracture			!	Stable
!	Dislocation fracture			!	Unstable

(Ogilvy and Heros, 1993; Sartor 2001)

1 At the time of injury. 2 Fracture of the ring of C1 due to compression between the occiput and C2. 3 May be overlooked if the dens is not displaced; sometimes stable. 4 Hangman’s fracture.

Table 37 Classification of traumatic transverse spinal cord syndrome (p. 274)

Loss of Function	Category	Features

Complete	A	No sensory or motor function, including in S4–5
Incomplete	B	No motor function. Sensory function intact below level of lesion,
		including in S4–5
Incomplete	C	There is motor function below level of lesion; most segment-in-
		dicating muscles have strength !3
Incomplete	D	There is motor function below level of lesion; most segment-in-
		dicating muscles have strength "3
None	E	Normal motor and sensory function

(American Spinal Cord Injury Association Impairment Scale; Ditunno et al., 1994)

Table 38 Treatment of spinal trauma (p. 274)

Result of Trauma	Treatment Measures

Neck sprain/whiplash in-	Analgesics, application of heat/cold, immobilization (as brief as possible). Early in-
jury	itiation of active exercise therapy. Measures to prevent chronification
Fracture	Stable conservative (extension/fixation). Unstable surgery
Arterial dissection	Anticoagulation
Spinal cord trauma	Methylprednisolone (i. v.) within 8 hours of trauma (bolus of 30 mg/kg over 15
	min, then 5.4 mg/kg/h for 23 hours). Monitor respiratory and cardiovascular func-
	tion, bladder/bowel function; thrombosis prophylaxis, pain therapy, careful
	patient positioning and pressure sore prevention. Transfer to specialized center
	for rehabilitation of paraplegic patients (as indicated)

				Appendix

Table 39 Clinical manifestations of spinal cord lesions (p. 282)

Features	Site of Lesion		Clinical Manifestations

Spinal cord transection	!	Cervical spinal cord	!	Quadriplegia
(p. 48)	!	Thoracic spinal cord	!	Paraplegia
	!	Lumbar/sacral spinal	! Paraplegia/conus syndrome with paralysis of blad-
		cord		der/rectum and saddle anesthesia
Lesion affecting a por-	!	Anterior root	! Flaccid paralysis, muscle atrophy, hyporeflexia (
tion of the spinal cord				segment-indicating muscles, see Table 2, p. 357)
(pp. 32, 50)	!	Posterior root	! Localized/radicular/referred pain, sensory deficit in
				corresponding dermatome
	!	Incomplete transverse	! Brown–Séquard syndrome, posterior column syn-
		cord syndrome		drome, anterior horn syndrome, posterior horn
				syndrome, central cord syndrome, anterior spinal
	!		!	syndrome
	!	Complete transverse	!	See p. 48
		cord syndrome
Temporal course	!	Acute	!	Spinal shock
	!	Chronic	!	Spasticity, sensory and autonomic dysfunction

Table 40 Malformations and developmental anomalies (p. 288)

Feature	Syndrome1	Comments2

Macrocephaly (ab-	Hydrocephalus (p. 290), hydranencephaly, megalencephaly	4th week/
normally large	(massively enlarged brain)	2nd to 4th month
head)
Craniostenosis	Turricephaly ( lambdoid and coronal suture; oxycephaly),	Before 4th year of life
(premature ossifi-	scaphocephaly ( sagittal suture; dolichocephaly, “long
cation of cranial	head”), brachycephaly ( coronal suture; “short head”)
sutures, p. 4)
Migration disorder	Schizencephaly (presence of cysts or cavities in the brain),	2nd to 5th month
(defective migra-	agyria (lissencephaly3, few or no convolutions), pachygyria
tion of neuroblasts	(broad, plump convolutions), heterotopia/dystopia (ectopic
into cortex)	gray matter)
Microcephaly (ab-	Micrencephaly (abnormally small brain)	5th week (primary),
normally small		perior postnatal (sec-
head)		ondary)
Dysraphism (neural	See p. 292	3rd to 4th week/
tube defect)		4th to 7th week
Chromosomal	Down syndrome (trisomy 21, mongolism), Patau syndrome	Genome mutation
anomaly	(trisomy 13), Edwards syndrome (trisomy 18), cri-du-chat
	syndrome (deletion, short arm of chromosome 5), Klinefelter
	syndrome (XXY), Turner syndrome (XO), fragile-X syndrome
Phakomatosis	See p. 294
Prenatal or peri-	Rubella, cytomegalovirus, congenital neurosyphilis, HIV/
natal infection	AIDS, toxoplasmosis
Mental retardation	A component of many syndromes (e. g., microcephaly, hy-
	drocephalus, Down syndrome, perinatal or prenatal infec-
	tion)
Cerebral lesion	Ulegyria (postanoxic corticomedullary scarring), poren-	Prenatal, perinatal or
	cephaly (p. 290), hemiatrophy, infantile cerebral palsy	postnatal
	(p. 288 f)

1 (Selected). 2 The times specified refer to the gestational and neonatal ages, respectively. 3 There are two forms of lissencephaly: type 1, Miller–Dicker syndrome (craniofacial deformity), and type 2 (pronounced heterotopia with Fukuyama muscular dystrophy).

Appendix

381

Appendix

Table 41 Age-related changes (p. 296)

Change	Sequelae		Elevated risk1 of

Accommodation	Presbyopia
Miosis	Light/convergence reaction
Cataract	Glare, visual acuity		Blindness
Hearing (inner ear)	Presbycusis		Deafness
Sense of smell/taste	Impaired sense of smell/taste
Body fat	volume of distribution for fat-soluble drugs2		Obesity
Total body water,		volume of distribution for water-soluble drugs2	Dehydration, hydro-
Thirst			penia
Arteries	Atherosclerosis, impairment of cerebral autoregula-		Stroke3, leukoaraiosis4,
	tion and blood-brain barrier, decrease in cerebral		subcortical arterios-
	blood flow, reduced tolerance of brain tissue to		clerotic encephalo-
	ischemia and metabolic changes		pathy (p. 172), cerebral
			amyloid angiopathy5,
			atrial fibrillation, myo-
			cardial infarction
Motor function	Mobility, reactivity, coordination, fine motor		Falls (p. 204), osteo-
	control, muscle atrophy (especially thenar, dorsal in-		porosis, fear of falling/
	terosseous, and anterior tibial muscles),		inactivity (avoidance of
	muscle force, leg muscle tone, hypokinesis of		social contact, isola-
	arms, gait impairment (p. 60)		tion)
Reflexes	Reflex movements (p. 42), palmomental reflex,		Falls
	snout reflex, grasp reflex
Sensation	Pallhypesthesia in toe/knuckle region, position		Polyneuropathy, ataxia,
	sense		falls
Brain atrophy	Senile forgetfulness6 (impairment of episodic		Alzheimer disease,
	memory, p. 134)		leukoaraiosis4
Cerebral dopamine syn-	Stooped posture		Parkinsonism
thesis
Cerebral norepinephrine			Depression
Non-REM stage 4	Early awakening, insomnia		Sleep apnea syndrome
(p. 112)

(Resnick, 1998)

1 Risk of developing condition in old age. 2 Increased risk of drug side effects. 3 Especially due to border zone infarction, subdural hematoma (after relatively minor trauma). 4 Rarefaction of white matter seen as bilateral, usually symmetrical hypodensity on CT and as hyperintensity on T2-weighted MRI (FLAIR = fluid-attenuated inversion recovery sequence). 5 Increased risk of spontaneous intracranial hemorrhage (p. 176). 6 Benign senescent forgetfulness, age-associated memory impairment (AAMI).

382

<<< < Предыдущая 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 3839 / 4539 40 41 42 43 44 45 > Следующая >>>

Соседние файлы в предмете Нормальная анатомия

#
11.08.201318.87 Mб201Color Atlas of Neurology.pdf
#
11.08.20133.26 Кб10Dirlister D_ANANOM 1.txt
#
11.08.201323.81 Mб26lubockii d n osnovy topograficheskoi anatomii.djvu
#
11.08.201327.86 Mб606Pocket Atlas of Sectional Anatomy, Volume 2 Thorax, Abdomen and Pelvis.pdf
#
11.08.201332.99 Mб45SURGICAL ANATOMY by Joseph Maclise.pdf
#
11.08.201314.01 Mб242Атлас. Нервная система человека. Строение и нарушения.pdf