Pattern of sensory abnormalities. Principal patterns of loss of sensation. (a) Thalamic lesion: sensory loss throughout opposite side (rare). (b) Brainstem lesion: contralateral sensory loss below face and ipsilateral loss on face. (c) Central cord lesion, e.g., syrinx: 'suspended' areas of loss, often asymmetrical and 'dissociated' , i.e. pain and temperature loss but light touch intact. (d) Hemisection of cord/unilateral cord lesion = Brown-Séquard syndrome: contralateral spinothalamic (pain and temperature) loss with ipsilateral weakness and dorsal column loss below lesion. (e) Transverse cord lesion: loss of all modalitiesm, including motor, below lesion. (f) Dorsal column lesion, e.g., MS: loss of proprioception, vibration and light touch. (g) Individual sensory root lesions, e.g., C6, T5, L4. (h) Polyneuropathy: distal sensory loss (Source: https://www.grepmed.com/images/3568/brownsequard-patterns-loss-diagnosis-bilaterality-neurology-sensory)
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Abstract
Anatomical localization means the site of lesion responsible for a patient's symptoms and signs. Neurological localization
requires a comprehensive understanding of anatomy and physiology of the nervous system. The process of localization
shall begin during history taking, may be refined during clinical examination, and shall be reassessed after relevant
diagnostic studies. Despite the advent and use of modern neuroimaging, nothing can replace a clinician's acumen to
localize based on history and examination.
165
Anatomic Localization of
Classical Neurological
Symptoms
Uddalak Chakraborty, Avik Mukherjee, Jyotirmoy Pal
Introduction
"I believe a neurologist who can happily spend 3
days examining a patient for challenging anatomical
localization will also be able to make a correct diagnosis
within 3 minutes in acute stroke. The most important
outcome of a neurological examination is anatomical
localization."1 Localization is derived from the Latin
word locus which means site. The diagnostic exercise of
determination of the site of nervous system affected by a
disease process, from the signs and symptoms, is termed
as localization in neurology.
Some authors argue that emphasis on anatomical
localization over years has hindered the development
of therapies in neurological diseases including epilepsy,
migraine, Guillain-Barré syndrome, Parkinson's disease,
multiple sclerosis and ischemic stroke, etc. However, the
diagnosis of idiopathic epilepsy, migraine, and Parkinson's
disease still remains clinical. Specialized neuroimaging
may have complemented the clinical diagnosis, but can
hardly replace it; there lies the importance of localization.
Common neurological symptoms can be localized
by meticulous history taking and appropriate clinical
examination, but sometimes one should be aware of false
localizing signs or symptoms, which may misguide the
clinician. In this chapter, we will try to localize lesions
based on a few common neurological symptoms.
Weakness
Weakness is a characteristic and common motor
neurodeficit, which may or may not be accompanied by
other symptoms per se. First of all, true weakness should
be differentiated from apparent weakness, either a vague
feeling of tiredness or even malingering which may present
like organic weakness. Proper clinical examination noting
especially the distribution of weakness, any distractibility
and a properly conducted Hoover's test may differentiate
between these. After identification of true weakness, it
should be categorized into an upper motor neuron type
(UMN) or lower motor neuron type (LMN) weakness,
differentiating features of which are given in Table 1.
UMN weakness predominantly affects extensors of
upper limbs and flexors of lower limbs.
Hemiparesis
Weakness of upper limb, trunk, and lower limb of one side
of body is usually the commonest presentation of stroke.
Chapter-165.indd 1 19-12-2020 14:03:14
2
Hemiplegia means complete loss of motor function on
that side.
Hemiparesis is usually due to involvement of
contralateral corticospinal tract (CST) from cerebral
cortex to lower medulla or ipsilateral CST in case of a
high-cervical cord lesion. Localization of hemiparesis is
demonstrated in Table 2. CST with possible sites of lesion
in hemiparesis has been shown in Figure 1.
Cruciate hemiparesis: Weakness of ipsilateral upper limb
with contralateral lower limb weakness is termed as
cruciate hemiparesis. The neuroanatomical explanation
involves the complex somatotopic and anatomical
segregation of the CSTs in the decussation at the lower
medulla oblongata or cervicomedullary junction. At this
level, the ventromedially located arm fibers decussate
rostral to the leg fibers, and a lesion at this specific point
can lead to this entity.3
False Localization in Hemiparesis
Kernohan's Notch Syndrome (Fig. 2) : A supratentorial
lesion may lead to transtentorial herniation of the temporal
lobe, with compression of the ipsilateral cerebral peduncle
against the tentorial edge; since this is above the pyramidal
decussation, this may lead to a contralateral hemiparesis.
Occasionally, the hemiparesis may be ipsilateral to the
side of lesion, and hence false-localizing; this occurs when
the contralateral cerebral peduncle is compressed by the
free edge of the tentorium.4
Monoparesis may be localized to cerebral cortex or
subcortex due to selective involvement representing that
particular limb.
Paraparesis
Weakness of both lower limbs may also be a common
presenting symptom. We have to differentiate UMN and
LMN type of lesions from history and clinical examination
(Table 3).
Features suggestive of myelopathy include a definite
level below which sensory modalities may be impaired/
absent; LMN weakness at the level of lesion and UMN
weakness below the level of lesion and bladder/bowel
disturbance.
Patient may complain a girdle-like sensation suggestive
of the sensory level of cord involvement. False localization:
Compressive lower cervical or upper thoracic myelopathy
may produce spastic paraparesis with a mid-thoracic
girdle sensation.5
Cerebral cause of paraparesis may be accompanied
by seizure, headache, etc. Cauda equina and conus
medullaris may be differentiated based on symptoms as
in Table 4.
Quadriparesis
Weakness of all four limbs; may be again categorized into
UMN and LMN (Table 5).
TABLE 1 Differentiation of UMN and LMN weakness based
on symptoms
UMN lesion LMN lesion
Tone Spastic Flaccid
Wasting Nil/Minimal Significant Wasting
Fasciculation Absent May be present
TABLE 2 Possible localization of hemiparesis
Site of lesion Features
Cerebral lesion
Complete hemiparesis:
Involvement of
same side of face
(predominantly lower
half) with ipsilateral
hemiparesis can be
commonly localized in
the internal capsule.
Contralateral cortex: Distal
predominant distribution of mild to
moderate weakness with seizures,
loss of cortical sensations, agnosia,
aphasia, etc.
Contralateral subcortical (corona
radiata): Faciobrachial weakness
with aphasia, homonymous visual
field defects.
Internal capsule: Dense hemiplegia,
hemianopia, hemianesthesia.2
Brainstem Cranial nerve palsy LMN type with
contralateral hemiparesis—crossed
hemiparesis
Ipsilateral Horner's syndrome due
to involvement of sympathetic
trunk. May also be seen in ipsilateral
thalamic lesions.
Ipsilateral hemiataxia due to
involvement of cerebellum and its
connections.
Cervical cord Ipsilateral hemiparesis sparing face
Ipsilateral loss of vibration and joint
position sense with contralateral
pain and temperature loss, usually
one to two segments below the
lesion (Brown-Sequard syndrome)
LMN findings at the level of lesion.
Chapter-165.indd 2 19-12-2020 14:03:14
CHAPTER 165 Anatomic Localization of Classical Neurological Symptoms 3
Fig. 1: Corticospinal tracts with possible levels
of lesion in hemiparesis
Fig. 2: Kernohan's notch syndrome
Sensory Abnormalities
Positive symptoms: Tingling (pins and needles), burning,
band like, itch, aching.
Negative symptoms: Numbness, difficulty in coordination
of limbs in dark places or closure of eyes (Table 6).
Pattern of sensory abnormalities have been shown in
Figure 3. Localization of sensory abnormalities are given
in Table 7.
Incoordination
In a patient with gait imbalance, we have to rule out any
nerve and muscle disorder, spinal cord or basal ganglia
disorder.
Localization of ataxia has been discussed in Table 8.
TABLE 3 Possible localization of paraparesis
Type of
lesion
Localization
UMN Central nervous system above lumbosacral cord.
Commonly in thoracic cord
Rarely in cervical cord
Occasionally, midline cerebral lesion like parasagittal
meningioma
LMN Conus medullaris
Cauda equina
Anterior horn cells in lumbar cord
Motor root of nerves of lower limb
Motor nerves of lower limb
Neuromuscular junction
Muscle
Chapter-165.indd 3 19-12-2020 14:03:15
4
TABLE 4 Cauda versus Conus medullaris
Cauda equina Conus medullaris
Pain Severe, asymmetric, radicular Less common
Sensory loss Asymmetric lower limbs, patchy Symmetric saddle anesthesia
Motor loss Asymmetric Symmetric
Sphincter involvement Less common and late Common and early
TABLE 5 Possible localization of quadriparesis
Type of lesion Localization Features
UMN Cervical cord
False localization:
Thoracic sensory level, paresthesia, clumsiness,
and atrophy of hands.
Cervical myelopathy:
Weakness of all muscles below a particular level.
Sensory loss below a circumferential level.
Sphincter disturbance
High cervical cord/foramen magnum:
Neck stiffness, suboccipital pain in C2 distribution.
Electric shock like sensation on flexion of neck.
Sequential weakness (Ehrlich's phenomenon)
Downbeat nystagmus, cerebellar ataxia (foramen magnum)
Onion skin pattern of sensory loss of face
Brainstem Cranial neve palsies, Horner's syndrome, Internuclear ophthalmoplegia
Brain (bihemispheric lesion) Pseudobulbar palsy (emotional lability/incontinence, spastic dysarthria)
LMN Anterior horn cells Pure motor weakness, prominent wasting, distal>proximal
Polyradiculopathy
False-localizing radiculopathy may occur in
Idiopathic Intracranial Hypertension and cerebral
venous sinus thrombosis and may manifest as
acral paresthesias, backache and radicular pain,
and less often with motor deficits
Predominant proximal weakness with sensory symptoms.
Polyneuropathy Distal symmetric weakness with sensory impairment in glove and
stocking distribution.
Neuromuscular junction Predominant proximal pure motor weakness with diurnal variation,
fatiguability.
Muscle Pure motor weakness without diurnal variation, fatiguability.
TABLE 6 Distribution of symptoms in reference to sensory
and autonomic bers
Fibers Symptoms
Small fibers Burning, painful dysesthesia, autonomic
dysfunction
Large fibers Sense of imbalance, limb incoordination,
tingling
Autonomic Postural dizziness, fainting, heat or cold
intolerance, sphincter dysfunction
Speech Disorders
A communication disorder in the form of slurred speech,
strained/effortful speech, monotonous low volume
speech, word finding difficulty, comprehension difficulty,
and naming problems should be recognized at first.7,8
Dysarthria as difficulty of articulation should be
segregated from aphasia; if dysarthria present, it may be
localized depending on the following types:
Spastic dysarthria: Pseudobulbar/UMN involvement
Flaccid dysarthria: LMN involvement
Chapter-165.indd 4 19-12-2020 14:03:15
CHAPTER 165 Anatomic Localization of Classical Neurological Symptoms 5
Fig. 3: Pattern of sensory abnormalities. Principal patterns of loss of sensation. (a) Thalamic lesion: sensory loss throughout opposite side
(rare). (b) Brainstem lesion: contralateral sensory loss below face and ipsilateral loss on face. (c) Central cord lesion, e.g., syrinx: 'suspended'
areas of loss, often asymmetrical and 'dissociated', i.e., pain and temperature loss but light touch intact. (d) Hemisection of cord/unilateral
cord lesion = Brown-Séquard syndrome: contralateral spinothalamic (pain and temperature) loss with ipsilateral weakness and dorsal column
loss below lesion. (e) Transverse cord lesion: loss of all modalitiesm, including motor, below lesion. (f ) Dorsal column lesion, e.g., MS: loss of
proprioception, vibration, and light touch. (g) Individual sensory root lesions, e.g., C6, D5, L4. (h) Polyneuropathy: distal sensory loss
Monotonous, hypophonic speech: Extrapyramidal
involvement
Clumping of syllables with undue separation: Cerebellar
involvement
Localization of aphasia may be done as follows:
Reduced fluency with difficulty in word finding and
impaired repetition: Broca's aphasia
Comprehension difficulty in terms of word and
sentences with impaired repetition: Wernicke's aphasia
Expressive and comprehension difficulty: Global
aphasia
Isolated repetition difficulty: Conduction aphasia
Preserved repetition with execution/comprehension
difficulty: Isolation/transcortical aphasia.
Visual Loss
First of all, one shall be able to differentiate between
decreased ability to see things, double vision or loss of
pieces of visual field.
Chapter-165.indd 5 19-12-2020 14:03:16
6
TABLE 7 Possible localization of sensory symptoms
Site of
lesion
Features
Cerebral
lesion
Cortex: Cortical sensation impaired. May affect
only a portion of contralateral part represented by
the affected homunculus.6
Internal capsule: Uniform involvement of
contralateral side with or without weakness.
Thalamus: Contralateral hemisensory loss;
contralateral hyperalgesia and allodynia (Dejerine-
Roussy syndrome).
Brainstem Contralateral side sensory involvement.
Ipsilateral sensory loss in face with contralateral
hemisensory loss in body—usually in lateral
medullary lesion.
Spinal
cord
Complete transection: Sensory loss below a level.
Spinal hemisection: Brown Sequard syndrome
(ipsilateral vibration loss and proprioception loss
with contralateral pain, temperature loss)
Selective dorsal (posterior column) or lateral cord
(spinothalamic tract) involvement.
Central cord: Suspended sensory loss with sacral
sparing; dissociative anesthesia.
Nerve
root
Focal symptoms depending on root of involvement
in a dermatomal pattern. Sensory symptoms may be
minimal in case of single root involvement, due to
considerable overlap by adjacent root territories.
Sensory
ganglion
Pure sensory involvement in non-length dependent
asymmetric fashion with sensory ataxia.6
Plexus Diffuse symptoms corresponding to two or more
adjacent roots usually associated with motor deficits.
Peripheral
nerve
Sensory impairment in the distribution of the affected
peripheral nerve; symmetric in case of polyneuro-
pathies or asymmetric in case of mononeuropathy/
mononeuritis multiplex.
TABLE 8 Possible localization of ataxia
Type of ataxia Features
Frontal Magnetic gait with out of proportion
ataxia, spasticity.
Sensory Paresthesia, numbness with
aggravation of symptoms in the dark,
high steppage gait.
Peripheral nerve (Large fiber):
Sensory symptoms in glove and
stocking distribution.
Dorsal root ganglion: Non length
dependent profound pure sensory
symptoms.
Posterior column: Definite spinal
level
Medial lemniscus: Brainstem
symptoms
Peripheral Vestibular Prominent vertigo with vomiting,
nausea, and relative sparing of speech.
Cerebellar
False localization
Frontocerebellar
pathway damage, may
result in incoordination
of the contralateral
limbs, mimicking
cerebellar dysfunction.7
Dysmetria, cerebellar speech, and
other symptoms, with or without
brainstem symptoms may localize
the lesion in cerebellum and its
connections.
Usually ipsilateral lesion leads to
ipsilateral symptoms.
Appendicular involvement
suggestive of cerebellar hemisphere
involvement, while truncal
involvement may be localized to
vermis; cerebellar speech due to
paravermal involvement; and a
combination of all may be seen in
pancerebellar disease.
Monocular visual loss is suggestive of lesion in the eye
itself or optic nerve anterior to the optic chiasma.
Binocular visual loss is suggestive of bilateral optic
nerve lesion or a chiasmal/retrochiasmal lesion.9
Visual loss correctable by pin hole/glasses: Refractive
error.
Visual loss not correctable by pin hole: Opacity in
ocular media/neurological illness.
Color Vision
Acquired disturbance of color vision is suggestive of optic
neuropathy and maculopathy; color desaturation being
one of the earliest manifestations of optic neuropathy.
Localization of visual loss has been shown in Table 9.
Pattern of involvement of visual field and their
respective localization has been shown in Figure 4.
Headache
Headache is one of the most common symptoms we
come across in our day-to-day practice. The pain sensitive
structures in the cranium which may give rise to headache
are as follows:
Scalp and aponeurosis
Middle meningeal artery
Dura mater and dural sinuses
Falx cerebri
Chapter-165.indd 6 19-12-2020 14:03:16
CHAPTER 165 Anatomic Localization of Classical Neurological Symptoms 7
TABLE 9 Possible localization of visual loss
Site of lesion Features
Ocular media Eye pain, lacrimation, redness, no improvement in vision with pin hole
Anterior visual pathway Monocular vision loss
Central scotoma/altitudinal field defect in one eye
Impaired color vision
Orbit: Isolated optic neuropathy
Optic canal/intracranial site: Other cranial nerves may be involved (III, IV, VI)
Lesions close to optic chiasma: Junctional scotoma
Posterior visual pathway Binocular visual loss
Homonymous/heteronymous hemianopia
Color vision may be impaired
Cortical defect Ventral occipitotemporal defect:
—Visual agnosia, prosopagnosia, topographognosia
Dorsal occipito-temporal defect:
—Akinetopsia, Simultagnosia, optic ataxia, ocular motor apraxia
Fig. 4: Localization of visual field loss
Chapter-165.indd 7 19-12-2020 14:03:17
8
Proximal segments of the large pial arteries
Cranial nerves V, VII, IX, and X
Cervical nerves C1, C2, and C3
Headache may result due to inflammation, traction,
compression, or malignant infiltration of these structures.
Primary involvement of these structures may give rise
to primary headaches, which have little localizing value,
while secondary involvement, for example, trauma, raised
intracranial tension may give rise to secondary headaches.
In case of an extracranial structure as the source
of headache, the site of pain is precise, for example,
inflammation of extracranial artery in giant cell arteritis
can be localized to the tender vessel.
Lesions of paranasal sinuses, teeth, eyes, upper
cervical vertebrae have less sharp localization, but pain is
referred in a regional distribution.
Infratentorial lesions tend to produce an occipitonuchal
distribution of headache, while supratentorial lesions
produce a frontotemporal headache.10
Among the primary headaches, cluster headache and
trigeminal cephalgias have a periorbital location while
migraine is usually unilateral and tension type headache
is bilateral in distribution.
Conclusion
In this chapter, the authors have tried to give an overview
of anatomical localization of a few classical neurological
symptoms. Despite the recent advances in neuroimaging
and electrodiagnostics, the importance and significance of
anatomical localization is still indispensable, as it can guide the
clinician to focus on a particular neuroanatomical substrate
and even cut the need of unnecessary extensive investigations.
We hope that this overview serves as a useful guide to the
clinicians in day-to-day practice.
References
1. Chaudhuri A. Localization in clinical neurology. Journal of the Royal
Society of Medicine. 2006;99(5):219. doi:10.1258/jrsm.99.5.219.
2. Ray BK, Approach to Hemiparesis, Bedside Neurology: Clinical
Approach, 1st edition. New Delhi: Jaypee Brothers Medical
Publishers; 2020. pp. 101-6.
3. Jeong HY, Chung EJ, Kim EG, et al. Anatomical findings of
hemiplegia cruciata in multiple sclerosis. Korean J Clin Neurophysiol.
2014;16(1):39-41. Available from https://doi.org/10.14253/
kjcn.2014.16.1.39
4. Kernohan JW, Woltman HW. Incisura of the crus due to contralateral
brain tumor. Arch Neurol Psychiatry. 1929;21:274-87.
5. Ochiai H, Yamakawa Y, Minato S, et al. Clinical features of the
localized girdle sensation of mid-trunk (false localizing sign)
appeared in cervical compressive myelopathy patients. J Neurol.
2002;249(5):549-53.
6. Ray BK. Approach to Peripheral Neuropathy, Bedside Neurology:
Clinical Approach, 1st edition. New Delhi: Jaypee Brothers Medical
Publishers; 2020. pp. 48-9.
7. Gado M, Hanaway J, Frank R. Functional anatomy of the cerebral
cortex by computed tomography. J Comput Assist Tomogr.
1979;3(1):1-19.
8. Lahiri D. Approach to Speech and Language Dysfunction, Bedside
Neurology: Clinical Approach, 1st edition. Ray BK (Ed). New Delhi:
Jaypee Brothers Medical Publishers; 2020. pp. 206-9.
9. Ray BK. Approach to Cranial Neuropathies, Bedside Neurology:
Clinical Approach. 1st edition. New Delhi: Jaypee Brothers Medical
Publishers; 2020. pp. 116-7.
10. Khadilkar SV, Soni GS. Headache. Neurology Simplified, 3rd edition,
New Delhi; CBS Publishers & Distributors Pvt Ltd; 2020. pp. 200-1.
Chapter-165.indd 8 19-12-2020 14:03:17
ResearchGate has not been able to resolve any citations for this publication.
Hemiplegia cruciata (HC) manifests as paralysis of the ipsilateral arm and contralateral leg. Herein, we report a 64-year-old man with weakness of the right leg and of the left arm after multiple sclerosis (MS). His brain and spine magnetic resonance imaging show a lower medulla lesion, which is extended to posterior part of C1 spine through cervicomedullary junction. HC usually results from stroke or trauma, but it is rare as presenting symptom of MS.
- J W KERNOHAN
- H.W. Woltman
The diagnosis of organic nervous diseases rests on a foundation built largely by anatomists, pathologists and physiologists. For this reason, it compares favorably in accuracy with diagnoses in other fields of medicine. In the localization of tumor of the brain, however, astonishing difficulties are often encountered. Thus, Magnan¹ (1878) reported a case of tumor and softening in the region of the left rolandic fissure, in which there were convulsive movements on the left side. The patient also had dementia paralytica and the marked meningo-encephalitis on the right side explained the convulsions on the left. Tucker² (1917) reported a case (case 4) of tumor of the left temporal lobe in which left hemiplegia was also present. Massive hemorrhage was noted in the right subcortical area. Meyer³ (1920) reported a case in which a supratentorial tumor had produced such marked herniation that the tentorial edge impinged on the right
-
![Mohamed Gado]()
- Joseph Hanaway
- Robert Frank
The authors describe the morphological characteristics that allow recognition of the individual computed tomography slice and determine its sequence in the series. In addition, each slices is "assembled" by defining the different cortical gyri, sulci, and cortical functional areas (based on Brodmann's maps). This work lays the foundation for correlative studies of location of lesions and the clinical picture.
-
![Richard Barohn]()
Neuropathic disorders encompass those that affect the neuron's cell body or neuropathies, those affecting the peripheral process, or peripheral neuropathies. The peripheral neuropathies can be broadly subdivided into the myelinopathies and axonopathies. These conditions can be hereditary or acquired. Each of these disorders has distinct clinical features that enable neurologists to recognize the various patterns of presentation. Once a particular pattern is established, further laboratory studies including electrophysiologic testing, nerve biopsy, and blood and cerebrospinal fluid examination can be performed to confirm the clinical impression. Therapy is available in some to correct the underlying disease state or at least to improve symptoms.
- Hidenobu Ochiai
- Y Yamakawa
- Seiichiro Minato
- Shinichiro Wakisaka
Cervical compressive myelopathy patients sometimes show localized girdle sensation in the mid trunk (so-called false localizing sign). This symptom often confuses physicians, but the clinical features and mechanism of this symptom are still unclear. We investigated the clinical features and possible mechanism. In each of five cases of cervical compressive myelopathy disease with and without mid-truncal girdle sensation, the clinical features, degree and shape of cord compression were analysed. The girdle sensation was expressed as a vague or burning sensation, and was localized with a width of 3 or 4 dermatomes from the T3 to T11 level. There was no correlation between the appearance of the girdle sensation and etiology and level of cervical cord compression. Pyramidal tract signs and disturbance of superficial sensation were observed in all cases. Furthermore, on axial MRI, the midline ventral surface of the cervical cord was remarkably compressed in cases with girdle sensation, as if the compressive lesion entered the anterior medial fissure of the cervical cord. From these findings, this false localizing sign may be caused by severe compression of midline ventral structure of the cervical cord. Ischemia of the thoracic watershed zone of the anterior spinal artery from the compression of the anterior spinal artery at the cervical level might also be considered to be a possible cause.
New Delhi: Jaypee Brothers Medical Publishers
- D Lahiri
Lahiri D. Approach to Speech and Language Dysfunction, Bedside Neurology: Clinical Approach, 1st edition. Ray BK (Ed). New Delhi: Jaypee Brothers Medical Publishers; 2020. pp. 206-9.
Approach to Cranial Neuropathies
- B K Ray
Ray BK. Approach to Cranial Neuropathies, Bedside Neurology: Clinical Approach. 1st edition. New Delhi: Jaypee Brothers Medical Publishers; 2020. pp. 116-7.
- S V Khadilkar
- G S Soni
Khadilkar SV, Soni GS. Headache. Neurology Simplified, 3rd edition, New Delhi; CBS Publishers & Distributors Pvt Ltd; 2020. pp. 200-1.
Source: https://www.researchgate.net/publication/350637854_Anatomic_Localization_of_Classical_Neurological_Symptomms
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