Avances en Neuropsicología (MUNC)

Dr. Fernando Ayuga Loro

Tema 3. Estructura y función del Sistema Nervioso

Contenidos

2
Objetivos

► Conocer las estructuras que componen el Sistema Nervioso

► Conocer las principales funciones de estas estructuras.

3
Introducción

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Avances en Neuropsicología RaquelFernando
Balmaseda
Ayuga
Serrano
Loro
Homúnculo de Penfield
346 PART I Common Neurological Problems

Medial TABLE 26.1 Cerebral Lesions

surface
Lesion
Location Symptoms Signs
Motor cortex Weakness and poor Incoordination and weakness
control of the affected that depends on the location of
extremity, which may the lesion within the cortical
involve face, arm, homunculus; often associated
and leg to different with neglect, apraxia, aphasia,
Lateral degrees or other signs of cortical
surface
dysfunction
Internal capsule Weakness that usually Often associated with sensory
affects the face, arm, impairment in same distri-
and leg almost equally bution
Basal ganglia Weakness and Weakness, often without sensory
incoordination on the loss; no neglect or aphasia
contralateral side
Fig. 26.1 Representation of the body on the Motor Cortex. Face and
Thalamus Sensory loss Sensory loss with little or no
arms are represented laterally, and legs are represented medially, with
weakness
cortical representation of the distal legs bordering on the central sulcus.

role of the basal ganglia in motor function, they are implicated in other as difficulty with motor control rather than hemiplegia or monoplegia.
functions, including memory and particularly the initiation, execu- Disorders with focal motor symptoms from basal ganglia dysfunction
tion, and termination of learned motor tasks (Packard et al., 2002). include Parkinson disease, dystonia, hemiballismus, and Huntington
There is also evidence of involvement of the basal ganglia in nonmotor disease.
cognitive tasks (Calabresi et al., 2016). Lesions of the cerebellum do not produce hemiplegia or monople-
Afferents to the basal ganglia are from the cerebral cortex and thal- gia. Instead, a lateral lesion will produce ipsilateral limb ataxia and a
amus to the striatum. Efferents from the striatum are largely to the glo- midline lesion gait ataxia.
bus pallidus and substantia nigra. The globus pallidus, in turn, projects
to the thalamus. HEMIPLEGIA
Cerebellum Cerebral Lesions
The cerebellum monitors and modulates motor activities, responding Cerebral lesions constitute the most common cause of hemiplegia.
to motor commands and inputs from sensory receptors of the joints, Lesions in either cortical or subcortical structures may be responsi-
muscles, and vestibular system. The cerebellum is somewhat topo- ble for the weakness (Table 26.1). Some lesions are both cortical and
graphically organized, with gait and axial musculature represented at subcortical, and some these can include mass lesions, infarctions, and
and near the midline and limb motor activity served laterally in the hemorrhages.
cerebellar hemispheres.
Cortical Lesions
Localization of Motor Deficits Cortical lesions produce weakness that is more focal than the weak-
The topographic organization of the cerebral cortex dictates that Fernando
ness seen with subcortical lesions. Fig 26.1 Ayuga
is a diagrammatic Loro
repre-
Lóbulos cerebrales

Fernando Ayuga Loro

Sistema motor: Vía córticoespinal

Fernando Ayuga Loro

Sistema sensitivo

Fernando Ayuga Loro

 Lenguaje
134 PART I Common Neurological Problems

Precentral gyrus Rolandic fissure

6
Postcentral gyrus
8 3, 1, 2
4
Parietal lobe

Inferior Supramarginal
frontal gyrus 46 gyrus
44
45 Angular gyrus
41, 42
19
Frontal lobe 22 Occipital lobe
47 18
38 21
Sylvian fissure 17
20
19 18
Superior
temporal gyrus
Temporal lobe

Broca’s area
Wernicke’s area
Fig. 13.1 The lateral surface of the left hemisphere, showing a simplified gyral anatomy and the relationships
between Wernicke area and Broca area. Not shown is the arcuate fasciculus, which connects the two cortical
speech centers via the deep, subcortical white matter.

last few decades based on numerous studies using the diverse method-
Right Left
ologies of cognitive neuroscience. Fernando Ayuga Loro
For both repetition and spontaneous speech, auditory information
Afasia sensitiva

Fernando Ayuga Loro

Vía visual
CHAPTER 13 Aphasia and Aphasic Syndromes 143

Right
visual
field

Left eye Right eye

Optic chiasm

Splenium

Angular gyrus

Left visual cortex

Fig. 13.6 Horizontal brain diagram of pure alexia without agraphia,
adapted from that of Dejerine in 1892. Visual information from the left
visual field reaches the right occipital cortex but is “disconnected” from
the left hemisphere language centers by the lesion in the splenium of
the corpus callosum.
Fig. 13.7 Fluid attenuated inversion recovery (FLAIR) magnetic reso-
nance image of an 82-year-old male patient with alexia without agraphia.
The infarction involves the medial occipital lobe and the splenium of the
corpus callosum, within the territory of the left posterior cerebral artery.

TABLE 13.7 Bedside Features of Pure TABLE 13.8 Bedside Features of Alexia
Alexia Without Agraphia With Agraphia
Feature Syndrome Feature Syndrome
Spontaneous speech Intact Spontaneous Fernando
speech Ayuga Fluent,
Lorooften some paraphasia
Ganglios basales

Fernando Ayuga Loro 12

Ganglios basales

Cuadro agudo de trastorno del movimiento

en extremidades izquierdas…

13
Ganglios basales

14
Ganglios basales

15
 Ipsilateral Contralateral

Movimiento ocular
Medial rectus
Superior rectus
Lateral rectus
Inferior oblique
Inferior rectus Superior oblique
A

Superior
oblique Superior rectus

Medius rectus

Inferior rectus

Fig. 18.8 A, Relationship

Lateral rectus muscles to x- and y-axes.
oblique muscles to the x-
Inferior oblique Von Noorden, G.K., 1985.
Ocular Motility, third ed. M
Fig. 18.7 The Six Extraocular Muscles for Each Eye.

inhibited (the Sherrington

The Final Common Pathway of Eye Movements ing the eyes to move con
The supranuclear networks send command signals to a “final common ing actions of the extraocu
pathway” that includes the ocular motoneuron, neuromuscular junc- planes of the semicircular
tion, and the final effector organ of eye movements—the extraocular vertical. These pulling acti
Fernando Ayuga Loro
muscle. For some time it was believed that all motoneurons and extra- insertions of the global laye
Diencéfalo. Tálamo

Fernando Ayuga Loro

Lesión talámica bilateral

Varón de 68 años, exfumador de dos paquetes diarios

desde hace 20 años e hipertenso conocido no tratado,
sin tratamiento activo.
Es traído a urgencias por su esposa por apatía, abulia
y bradicinesia de dos días de evolución y comienzo
brusco.
El estudio neuropsicológico demostró ligero déficit en la
capacidad mnésica, presentando fallos en la capacidad
de fijación y en la evocación categorial.
No presentaba ninguna focalidad neurológica.

Ictus de arteria de Percheron

Fernando Ayuga Loro

Tronco encefálico

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Avances en Neuropsicología RaquelFernando
Balmaseda
Ayuga
Serrano
Loro
Motilidad pupilar
CHAPTER 17 Pupillary and Eyelid Abnormalities 193

Short ciliary nerve

Parasympathetic Ciliary to ciliary muscle
efferent fibers ganglion
III
Midbrain

V
Long ciliary nerve
to dilator pupillae

Carotid plexus Short ciliary nerve

Medulla to sphincter pupillae
Postganglionic
fibers
I. C.
Superior cervical
ganglion

I. Th.
I. Thoracic ganglion
II. Th.

Sympathetic efferent
(preganglionic) fibers
Fig. 17.2 Parasympathetic and sympathetic pathways for innervation of the sphincter pupillae and dilator
pupillae. I. C., First cervical spinal cord segment; I. Th., first thoracic segment; II. Th., second thoracic seg-
ment; III, oculomotor nerve; V, trigeminal nerve. (Adapted from Gray, H., 1918. Anatomy of the Human Body,
plate 840.)

Anisocoria Greater in the Light

Fernando
may also be seen as a componentAyuga Loro
of a systemic autonomic neuropathy
Postganglionic parasympathetic dysfunction—tonic pupil. (see Chapter 107) (Bremner and Smith, 2006; Yamashita et al., 2010),
Pupilas

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Avances en Neuropsicología RaquelFernando
Balmaseda
Ayuga
Serrano
Loro
Lesión troncoencefálica

Mujer de 55 años acude por

mareo y diplopia vertical de 5
horas de evolución…

Fernando Ayuga Loro

Coordinación ocular

CHAPTER

Gaze left

LE CN III RE

3 3

MLF
6 6
+ –
CN VI PPRF

Ampulla
+ +
Horizontal
semicircular
canal
VN

Fig. 18.6 A lateral head turn (yaw, or side to side) induces movement
of the endolymph in the ipsilateral horizontal semicircular canal toward
the ampulla (as would warm water caloric stimulation of the external
auditory meatus/tympanic membrane) and thus excites the contralat-
eral abducens nucleus and inhibits the ipsilateral abducens nucleus via
the vestibular nuclei (VN). Each abducens nucleus innervates the ipsi-
lateral lateral rectus muscle via the abducens nerve and the contralat-
eral medial rectus muscle via the abducens nucleus interneurons, the
medial longitudinal fasciculus (MLF), and the neurons for the medial rec-
tus (part of cranial nerve [CN] III nucleus). Neurons in each paramedian
pontine reticular formation (PPRF) also have an excitatory input to the
ipsilateral abducens nucleus and an inhibitory input to the contralateral
abducens nucleus for saccades and quick phases of nystagmus. LE,
Left eye; RE, right eye. (Adapted from Lavin, P.J.M., 1985. Conjugate
and disconjugate eye movements. In: Walsh, T.J. [Ed.], Neuro-ophthal-
mology: Clinical Signs and Symptoms. Lea & Febiger, Philadelphia.)
Fernando Ayuga Loro
Consciencia CHAPTER 6 Prolonged Comatose States and Brain

Diencephalon
(thalamus and Persistently
hypothalamus) Comatose
Cortex
Consc

PVS MCS CM

MCS(L)

MCS(NL)

Fig. 6.2 A concept of categories of persistent

ness. (See text for explanation.) CMD, Cogn
HMD, higher-order cortex-motor dissociation
scious state; PVS, persistent vegetative state.

The clinical assessment of a patient who is

challenging (Fig. 6.2). The examination may n
Ascending Reticular
Activating System (ARAS) ferent times of the day because of fluctuations
(midbrain and upper pons) dian oscillations affecting arousal. Some studie
in a substantial minority of patients in PVS
13%–28% of supposedly vegetative patients u
Fig. 6.1 Key structures in maintaining an awake state and awareness. as the Full Outline of UnReponsiveness (FO
(From Wijdicks, E.F., 2014. The Comatose Patient, second ed. Oxford Recovery Scale-Revised (CRS-R) (Giacino et a
University Press, New York.) 2009; Wijdicks et al., 2005). Diagnostic error
cited, but this frequency might be falsely high
based on poor reporting standards and insuffi
at autopsy showing extensive damage to the subcortical white matter 2018).
or thalamus, with sparing of the brainstem (Adams et al., 2000).
At what point can a vegetative state (VS) be considered permanent? Minimally Conscious State
Fernando Ayuga
When is there a high degree of clinical certainty that the clinical state InLoro
the 1990s, clinicians involved in the care o
Formación reticular ascendente

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Avances en Neuropsicología RaquelFernando
Balmaseda
Ayuga
Serrano
Loro
Cerebelo

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Avances en Neuropsicología RaquelFernando
Balmaseda
Ayuga
Serrano
Loro
Cerebelo

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Avances en Neuropsicología RaquelFernando
Balmaseda
Ayuga
Serrano
Loro
Médula espinal

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Avances en Neuropsicología RaquelFernando
Balmaseda
Ayuga
Serrano
Loro
 Dermatomas CHAPTER 31 Sensory Abnormalities of the Limbs, Trunk, and Face 40

C2
C3

C8 C6 C7
C7 C5

T4

C8 C8
T10

T10
S2
S3
L1 L1
S4
S2–S4
S1
L3 L3

S1

S1 L5

Fig. 31.3 Dermatomes: Cervical (C), Thoracic (T), Lumbar (L), and Sacral (S). Boundaries are not quite as
distinct as shown here because of overlapping innervation and variability among individuals. (Reprinted with
permission from Martin, J.H., Jessell, T.M., 1991. Anatomy of the somatic sensory system. In: Kandel, E.R.
(Ed.), Principles of Neural Science. Appleton & Lange, Norwalk, CT.)

describes the clinical situation in which sensory loss involves a number in patientsFernando
with intrinsic spinal
Ayuga cord lesions such as tumors, but it ca
Loro
Sueño CHAPTER 101 Sleep and Its Disorders 1683

Organization
Pineal A
gland

C
Retina
Dark +
(Stimulation of +
Melatonin Production) –
+
Raphe
Retina RHT s
nucleus NA
B
(GLU)

SCN –
SCG
MT1 , MT2
5-HT2C
+
–
Light receptors
(Inhibition of
Melatonin Production)
Circadian rhythms
(e.g., hormones,
core temperature, Modulation
sleep, appetite) (e.g., mood,
meals, work
sleep, activity)

Fig. 101.20 The Suprachiasmatic Nucleus Sends Timing Information to the Brain and Periphery. The
circadian pacemaker is located in the hypothalamic suprachiasmatic nucleus (SCN). It is responsible for gen-
erating the internal circadian rhythms in gene expression, electrophysiology, and hormone secretion. Direct
projections from the retina carry information about the cycle of light and darkness to the SCN, which in turn
synchronizes a phase of SCN rhythms with the external environment. (FromFernando
de Bodinat, C., Ayuga Loro
Guardiola-Lemai-
Bibliografía

https://neurorecordings.com/

31
Bibliografía

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Avances en Neuropsicología RaquelFernando
Balmaseda
Ayuga
Serrano
Loro
Bibliografía

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Avances en Neuropsicología RaquelFernando
Balmaseda
Ayuga
Serrano
Loro
Recursos

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Avances en Neuropsicología RaquelRaquel
Balmaseda
Balmaseda
Serrano
Serrano
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Avances en Neuropsicología Raquel Balmaseda Serrano
Bibliografía

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Recursos

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