International Health

a report by
Karin E
Upper debol
Eeg-Ol
Motor ofsson
Neuron
Associate Professor, Institution of
Disord
Neuroscience, Section of Clinical
Neurophysiology, University
ers inUppsala, Sweden
Hospital
DOI:10.17925/ENR.2008.03.02
Africa .117

including throug v
speaking, h the
Mot
walking, ventral
i
or
breathing, roots e
neu
swallowing andto the
ron w
general muscle
diso
movement ofcells
rder
the body.lead to i
s
MNDs areweakn
(MN
generally ess
s
Ds)
progressive, and t
are
but there aremuscle
a o
exceptions. Inatroph
gro
upper MNDs,y. d
up
cells in theExamp
of e
motor cortex ofles of
neu s
the brain areMNDs
rolo
gica
affected, asare c
well as theirgiven
l ri
projections inin
diso
the Table b
rder
corticospinal 1.
s in e
tract. Signs of
whi c
upper motor
ch
neuron T li
mot
damage
or h n
include
neu
muscular e i
rons
weakness,
are m c
spasticity, brisk
dest
reflexes and a a
roye
the Babinski i l
d.
sign. In
Mot
addition, some
n a
or
subjects exhibit a n
neu
cognitive
rons i d
changes, and a
are
small m n
larg
proportion
e e
exhibit
cell o u
frontotemporal
s
that
dementia.1 In f r
contrast,
cont t o
degeneration of
rol
neurons h p
volu
ntar
located in the i h
ventral horns of
y s y
the spinal cord
mus
cle
(lower motor r s
neurons) with
acti e i
projections
vity,
 cific
olo uppercharac person
MNDs interised ,
gic by a showin
Africa
al
mentioned sudde g
below, theren bilater
fin
are alsoonset ally
din
disorders withof a exagg

gs
both upperspastic erated
and lowerparapa knee
in
motor neuronresis and/or
kon
symptoms, or ankle
such
zo, asquadri jerks
amyotrophic paresi without
alateral scleros.s in signs
Below, a puresevere
non of

lower MND,ly diseas

-
poliomyelitis, affecte e of
pro
is mentioned,d the

since
gre poliosubject spine.”

immunisation s. In
10

ssi
campaigns 1996, Criteri
ve
are highlythe a for
topical inWorld the
upp
Africa. As aHealth degree
er Organi of
differential
zation severit
diagnosis
mo to
(WHO) y of
MND, tropical
tor
ataxic
sugge konzo
sted accord
neu
neuropathy
the ing to
(TAN) is
ron followi the
mentioned.
dis ng WHO
The main aim
diagno are:
of this
ord review
stic mild
is to describe
ers
clinical and
criteria form –
for subject
rep
neurophysiolo
konzo: is able
gical findings
ort “a to walk
in konzo, a
visible
ed
non- without
symm suppor
progressive
in etric t;
upper MND
sev
reported in
spastic moder
abnor ate
eral
several
mality form –
remote rural
re when subject
areas of the
walkin uses
mo
Central
g one or
African
te and/or two
Republic,
rur runnin sticks
Mozambique,
g, a to
al
Tanzania and
history walk;
the
are of and
Democratic
abrupt severe
as
Republic ofonset
form –
Congo
of (<1 subject
2–9
(DRC). week),
Afr is
a non- unable
ica.
Upper Motor progre to
Neuron
Disorders in ssive walk.10
Africa course
Apa Konzo was first ; onset
rt described in in a
1938 in the
fro Bandundu formerl
m province of the y
2
the DRC. health
spe It is
y
 the Yaka ethnicappear the
group of thein legs or
In
Bandundu conne in the
addi
province in thection lumbar
tion
DRC andwith area.
to
means ‘tiedfood Weakn
mot
legs’, referringshorta ess of
or
to theges the
sym
scissoring gaitand lower
pto
of affectedfamine extrem
ms,
13
som subjects. s. 21–25 ities
e Epidemiologica then
Neurol
affe l studies haveathyris develo
cted shown that them has ps,
subj disease is
been leadin
ects associated with g to a
around
may a high spastic
for a
pres exposure to parapa
very
ent cyanogenic resis
long
with compounds in that in
time,
blur a diet
and some
red dominated by
epide subject
visi insufficiently
mics s gives
on, processed
have a
nyst bitter
occurr severe
agm cassava.14–18
ed in disabili
us Persons
areas ty with
and consuming
spe poorly such compl
ech processed as ete
depen
diffi cassava inIndia,
culti large quantitiesthe dency
es are susceptibleMiddle in
of East, activiti
to
pse es of
neuropathologi Russia
udo daily
es caused byand
bulb southe living.
cyanide.19,20
ar rn
type Affected Tropica
Europ
subjects also
.11 26,27 l
The
have a lowe.
spastic
dise intake ofNeurol
parapa
ase sulphur aminoathyris
mai m resis
nly acids, which (TSP)
affe are needed toaffects
cts more is a
chil detoxify men slowly
dre cyanide in the
n than progres
and human wome sive
wo body.14–20
n, and, spastic
men
of as in parapa
chil Neurolathyrism konzo, resis
dbe is another toxic
arin young with an
g nutritional age is insidiou
age. disorder knownassoci
10,12 s
in Africa. It isated
Kon an irreversible onset.
with an TSP
zo spastic
increa
is paraparesis mainly
sed
nam affects
caused byrisk of
ed adults
excessive paraly
afte living in
consumption of
r a sis.25 tropical
grass peas
loca At
(Lathyrus and
l onset
sativus). subtrop
desi there
Neurolathyrism ical
gnat are
is known in areas
ion often
Ethiopia, where of the
amo cramp
neurolathyrism world,
ng s in
epidemics for
exa une-mediated needle In
mpl inflammatory s and additio
e disease sexual n to
Wes associated withcontact neurolo
tern infection with. TSP gical
Afric human T-causes sympto
a, lymphotrophic muscle ms,
regi virus 1 (HTLV-1);weakn subject
ons this associationess, s with
of was firststiff
Sout reported in 1985muscle
Karin Edebol Eeg-
h by a Frenchs and an Associate Profe

Ame group.28 TSP ismuscle University Hospital

In 2007 she was
rica transmitted spasm Professor at the U
and person tos, Sydney. She is Edito
Paediatric Clinical
the person viasensor
Neurophysiology, an
Cari infected cells;y special interest in ha
bbe the virus can bedisturb disorders in children
and medicine in dev
an. spread throughance
countries. She studie
TSP the placenta,and at the Universities of
is abreast-feeding, sphinct and Linköping, and s

syst blood er in paediatric neurolo

University of Gothen
emictransfusions, dysfun
imm contaminated ction. E: karin.edebol.
olofsson@akad
e

©
TO
UC
H
BR
IE
FI
NG
S
20

08
11
7
International Health
ALS = documented
amyotr
cases of
ophic
lateral TSP/HAM
Table scleros
among
1: is; PLS
Exam = children and
ples primar adolescents.35
y
of
lateral The juvenile
Motor scleros
Neuro is; form of the
n SMA = disease is
Disordspinal rapid and
ers muscul
ar more
atroph progressive
Phenotype
y.
than the adult
UMN + LMN
form. In
TSP may
addition to
suffer from
UMN myelopathy,
uveitis or
12 of the
keratoconjunti
children and
vitis sicca,
adolescents
arthritis,
also
pulmonary
Bulbar presented
alveolitis,
LMN focal with chronic
polymyositis
Primary infective
and
dermatitis
dermatitis.
Secondary associated
Some HTLV-1
with HTLV-I
subjects
LMN regional 34
develop (IDH). Dual
leukaemia or infection with
29– HTLV-I
lymphoma.
LMN general
32
TSP/HAM and
TSP affects
HIV-1 has
U mainly adults
M been found in
between 30
N some
and 40 years
=
subjects;
of age and is
HTLV-I and
u considerably
HIV-I are both
p more common
p retroviruses
e in women
and share
r than in men.
similar routes
m
In 1986, a
of
o syndrome
t transmission.3
similar to TSP
o 6
r was reported Oral or
in Japan, and intravenous
n
e was named corticosteroid
u HTLV-1- s are the main
r
associated treatment of
o
n myelopathy TSP/HAM,
; especially in
(HAM).33 In
L the initial
1988, the
M phase, but
N WHO
other drugs –
recommended
= for example
both
valproic acid,
l syndromes to
o methotrexate
be grouped
w and
e together
r interferon-
under a
alpha – are
m common
o also
name,
t suggested if
34
o TSP/HAM.
steroids fail or
r Although
cannot be
n TSP/HAM is
32
e used.
not common
u
r in younger
o ages, up to
n
2006 there In contrast
;
were 17 well- to the upper
MNDs of age of polio in
(konzo 6%, with
, female
neurol dominance
athyris (7.7%
m andversus 3.9%
TSP/H in males).37
AM), The highest
TAN isage-specific
predo prevalence
minant was found
ly ain elderly
sensor women.
y TAN is
neurop linked to
athy consumptio
freque n of
ntly cassava
seen foods.
in
malno In connection
urishe with MNDs
d and Africa,
popula poliomyelitis,
tions.
a lower
Sympt
motor neuron
oms of
syndrome,
TAN
must be
include
mentioned.
bilater
In 1988, the
al optic
WHO
atroph
decided to
y,
take action to
bilater
eradicate
al
neuros polio by

ensory 2000.
deafne Despite
ss, much
sensor progress in
y gaitreducing the
ataxia incidence of
and polio, it still
symm exists –
etrical mainly where
sensor there is
y poverty.
polyne However, the
uropat number of
hy. polio-
Screenendemic
ing forcountries has
TAN indecreased
a from 125
Nigeriacountries in
n
1988 to four
comm
in 2006
unity
(Nigeria,
showe
India,
d an
Pakistan and
overall
Afghanistan).
preval
In 2006,
ence
Namibia
from
experienced
10
its first
years
outbreak of
 first affected
description persons.41,42
2–
more by Trolli. A few
than 4,6,12,40,41 patients
10 Konzo has a experience a
years.3 sudden certain
8 improvement
onset of gait
Anoth difficulties, after the
er often acute phase,
outbre preceded by and
ak thereafter a
prolonged
occurr
physical non-
ed in
exercise. progressive
Kenya
Spasticity is disability.
during
Aggravation
2003– present
2006, from the may appear
and onset. Most with
led tosubjects continued
a experience consumption
nation trembling or of cassava,
al andcramping in and
interna the legs at manifests as
tional onset and/or
a sudden
spread
heaviness onset of
, with
and pain in symptoms of
re-
the legs. the same
infectio
Some type as
n of 20
polio- subjects initially seen
free report in konzo,
countri paresthesia, leading to a
es.39 electrical permanent
Large- discharges change for
scale in the legs the worse.
emerg and low- The
ency back pain at symptoms of
polio onset;
konzo vary,
immun however,
with the the
isation these
mildest form
campa
symptoms manifesting
igns
resolve as the ability
were
within a few to walk
thus
directe weeks. Most without
d topatients are support with
high- initially no overt
risk confined to lower limb
countri bed, and
weakness,
es. thereafter
but with
try to walk.
signs of
Clinic Blurred
exaggerated
al vision,
Findin deep tendon
gs in speech reflexes in
Konzo and/or
the lower
swallowing
limbs. The
Onset difficulties
majority of
The may be
affected
clinical experienced
konzo
picture at onset.
subjects
of
experience
konzo Motor
Symptoms various
has
and Signs degrees of
been
Konzo has a symmetric
well
stable clinical weakness of
charac
course after the lower
terised
onset in the extremities,
since
majority of with a
the
spastic visual acuity. abnormal
gait, Neuro- findings.44
and aophthalmolo Co-
few gical studies ordination is
also have normal, and
have confirmed there is no
weakn the presence sign of
ess ofof optic
cerebellar
the neuropathy
dysfunction.
upper in konzo
Hearing is
patients, with
limbs normal.
visual
and the Other than
impairment,
trunk. experiencin
defect of
Some g electric
visual fields
person discharges
and temporal
s are in the lower
pallor of the
non- limbs at
optic discs.43
ambula onset of
Rotatory
nt. konzo, there
nyastagmus
Ankle are no
is seen in
clonus sensory
some
is symptoms.
affected
freque There are
people.
nt, no
Among
Babins symptoms
moderate
ki sign of
and severely
is autonomic
disabled
present konzo dysfunction
and in konzo:
subjects,
palmo some have urinary,
mental dysarthria bowel and
and sexual
due to
cutane pseudobulba functions
are normal.
ous r palsy.41 The
abdomi motor
nal Neurophysi
disability ological
reflexe may, due to Findings in
s aredisuse, give Konzo
often rise to
present muscle Backgroun
. atrophy. d
In 1998 and
Additi Normal 2000, our
ve Features research
Sympt Konzo group from
oms
and subjects the
Signs have normal University
Some cognitive Hospital in
konzo function Uppsala
patient even when brought
s electroence high-tech
report phalogram equipment
impaire (EEG) to the DRC
d shows in order to

118
EUR
OPEA
N NE
URO
LOGI
CAL
REVI
EW
Upper Motor Neuron Disorders in Africa
June 2000, the
study continued in All five subjects
neurophysiolo the same way with the severe
gically with another 15 form of konzo had
investigate konzo subjects, of a general slowing
konzo patientswhom five also of background
and healthyunderwent activity, three of
relatives. muscle biopsy. A the six subjects
Konzo patientsgeneral with the moderate
and relativesdesciption of the form had the
were recruitedtwo study groups same EEG
from villages inof konzo subjects findings and in
the Bandunduis shown in Table four of the 10
province, 500–2. subjects with mild
600km south- konzo
east of theElectroencephal background
ogram activity was
capital,
EEG during slowed. All
Kinshasa,
wakefulness was relatives, except
where they
recorded in 21 for one, had
were
konzo patients and
hospitalised at normal EEG
13 of their
the findings; in the
relatives.44 The one abnormal
neuropsychop
EEG recordings EEG there was
athological
were abnormal in episodic
centre at the
12 konzo patients generalised
University
(57%) 10–49 years slowing.
Hospital during
of age (median
the study. Two
15.5 years), with a
nurses, active
disease duration of I
in the
three to 11 years
catchment n
(median six years).
area in
Eight patients had
Bandundu and
general slowing of
speaking the 1
the background
tribal language 9
activity. Of these,
of the
participants,
two had frontal 9
dominance of the
stayed in the
slowing, four had
8
hospital with
general episodes
them for
with slow activity
support. All a
and four had focal
participated
slowing (frontal n
after informed
and centroparietal d
consent and
leads,
community
respectively).
acceptance. 2
Three konzo
patients had 0
Over four
slowing of the post-
weeks in Julycentral rhythm,
0
1998, 21consisting of theta 0
konzo subjectsactivity at a
underwent
,
frequency of 6–
neurological 7Hz and absence
examinations, of alpha activity.
o
neurophysiolo Reactivity, with
gical andvisual u
blocking,
ophthalmologi was normal in all r
cal patients. No
investigations epileptiform
and laboratorydischarges were
r
tests of bloodseen in the e
and urine. Inpatients.
s
e t r
a h o
r e p
c h
h D y
e s
g m i
r o o
o c l
u r o
p a g
t i
b i c
r c a
o l
u R l
g e y
h p
t u i
b n
h l v
i i e
g c s
h t
- o i
t f g
e a
c C t
h o e
n
e g k
q o o
u i n
i n z
p o
m o
e r p
n d a
t e t
r i
t e
o t n
o t
t s
h n
e e a
u n
 d time.49 MEPs
after TMS were
recorded Table
h bilaterally in hand 2:
and lower limb Desc
e riptio
muscles
a n of
(abductor digiti
Konz
l minimi and tibialis o
anterior, Subj
t respectively) in 14 ects
Inves
h konzo subjects.49
tigat
Motor responses
y ed in
in hand muscles 1998
were obtained in and
only five of 14 2000
r
subjects; all five
e had clinically
Number
l preserved
Females
a Males
Age (years)
t Mean
i Median
Range
v Height (cm)
Mean
e
Median
s Range
Weight (kg)
.
Mean
Median
Range
Motor-evoked
Potentials Duration of konzo (years)
Median
To elucidate
Range
motor
Degree of severity
pathways in
Mild
konzo, Moderate
patients were Severe
investigated Type of konzo
with Symmetrical spastic paraparesis
transcranial Tetraparesis
electrical Babinski sign
stimulation
(TES) in 1998,
and with upper limbs.
transcranial Motor responses
magnetic were absent in
stimulation nine subjects, in
(TMS) in whom responses
2000. 46–49 could be obtained
Motor-evoked after voluntary
potentials contraction
(MEPs) after (facilitation). In
TES, recorded lower limb
in hand muscles, motor
muscle responses were
(abductor absent in 13
pollicis brevis), subjects, and in
were normal in one there was a
two out of 21 very low
patients,
amplitude
abnormal in 10
response. The
and absent in
abnormal TES
nine. The
findings in almost
abnormality
all konzo patients
consisted of
suggest abnormal
prolonged
central conduction in
conduction descending motor
pathways, andcortical latencies four and
the abnormalin six subjects. prolongation of
TMS findingsMedian nerve cortical latencies
are consistent SEPs, on the in two. The SEP
with cortical other hand, were abnormalities are
and/or sub-normal in 19; in not correlated to
cortical two subjects there occurrence of
abnormalities. were no cortical sensory
responses. symptoms at
Somatosenso onset or to the
ry-evoked In a study in duration or
Potentials 2000, median severity of konzo.
Involvement ofnerve SEPs were
somatosensor normal in 12 of 15
Visual-evoked
y pathways,patients, whereas Potentials
especially in
in three no The neurodamage
the lower
cortical responses in konzo also
limbs, has
were obtained. Of involves the visual
been shown in
12 tibial SEPs, pathways. Visual-
konzo.50 In our evoked potentials
only three were
1998 study, all (VEPs) were
normal. In nine
investigated recorded in a study
subjects with
subjects of 23 konzo
abnormal tibial
(n=21) had patients and in 38
SEPs, there was
abnormal tibial
bilateral absence healthy subjects.51
somatosensor
of cortical VEPs were
y-evoked
responses in abnormal in 11
potentials
three patients, patients, with
(SEPs), with
unilateral prolongation of
absent cortical
P100, absence of
responses inabsence of
cortical response P100 in two and
15 and
with prolonged atypical waveform
prolonged
cortical latency in in

EUROPE
AN NEU
ROLOGI
CAL RE

VIEW
119
International Health
s,
Electromyo
graphy and
anothe Muscle Concentric
r twoBiopsy needle
subjectIn 1998, the electromyogr
s. Sixfirst study of aphy (EMG)
of theperipheral was normal
patient nerves in in all
s withkonzo investigated
abnor subjects patients
mal was (n=21), with
VEPs performed no
had (not
neurogenic
normal counting signs.
visual two patients Muscle
acuity. who were
biopsies from
The investigated
five konzo
mean at the
patients
Neurophysi
P100
ological revealed
latency
Laboratory non-specific
was
in Uppsala changes
signific
at the secondary to
antly
beginning of muscle
increa
the 1990s). waste.
sed
Twenty-one
and
konzo Comments
the on the
subjects
P100 Neurophysi
nine to 49 ological
amplit
years of age Findings in
ude Konzo
(median 17
signific Although
years, mean
antly the
22 years)
decrea participated neurophysio
sed inin the study. logical
konzo Surprisingly, investigation
patient considering s indicate a
s that the more widely
compa konzo distributed
red subjects cortical and
with were subcortical
health malnourishe dysfunction
y d, no patient in konzo,
control showed any the exact
s. Thesigns of site of lesion
abnor polyneuropa in konzo
malitie thy.45 Motor remains a
s inand sensory challenge.
konzo nerve The
patient conductions predominant
s dowere motor
not normal. features in
correla konzo
te to indicate a
duratio prepondera
n or nt
severit vulnerability
y of in the motor
konzo. cortex
pyramidal
Nerve cells;
Cond
uction however,
Studie whether the
 lesion r. Abnormal level of
is pre-MEPs, cyanogenic
synaptiSEPs and compounds
c, VEPs have and their
neuron also been metabolites,
al ordescribed in and MEPs
post- other upper of various
synaptiMNDs. kinds, are
c, or aFurther needed to
combi studies, in further our
nation regard to understandi
of both ng of the
these, neuropathol pathogenesi
is ogy, effects s of konzo.
unclea on cellular ■
des laborato st 10 ala D,
observat ry u 2– Saute
ions findings di 8. F, et
réunies, in e al.,

1. Jose au patients, d
8. Ty Konz
Kwango, Bul in lle o
phs
au sujet l Ta sk assoc
KA,
de deux Wo nz är iated
Dick rld
affection a T, with
son He L
DW,
s
alth ni war
d’origine Or a, é in
Fron
indéterm ga B g Moza
tote
inée, n, ra u mbiq
mpo 198
Brussels in, é ue,
ral 4;6
F,
loba
: Fonds
2:4 1 Trop
Reine 77– 9 P Med
r
Elisabet 84. 9 et Int
deg
er
ener
h;
1938;1–
5. Cliff J,
0;
11 so
Healt
h,
ation Lundq 3:
36. n 1997;
with uist P, 2 S,
3.
upp Lucasse Mårten 2 et
2:106
8–74.
er sson J, 3
C, Le al.
mot
or
“Kitondji et al., – , 10. W
”, Associ 3 K HO,
neur ation Konz
synony 5. o o, a
on of high
me le nz distin
dise
“Konzo”,
7. How
cyanid o ct
ase/ type
un e and lett in of
prim low W, upper
paralysi th
ary moto
e sulphu Bru e neuro
later r bak
spastiqu C n
al intake er disea
e, Ann e
scler se,
Soc in G, nt
osis, W
Belg cassav Mlin ra
Neu k
Med a- gi l l
rolo induce N,
Trop, Af y
gy, d Rosl
1952;33 ric
200 spastic ing E
:393– a
7;69 p
401. parapa H, A n
(18): i
resis, geo R d
4.
180 Ministry Lancet grap e e
0– , hica m
of p
180 1985;ii l i
Health u
1. o
Mozamb :1211– clus bli l
2. Trolli ique, 13. ter
of
c, R
G,
Mantaka
ssa: an
6. Howl kon
N
e
e
c
Para ett ,
epidemi zo ur
plégi WP, 1
c of in ol
e Brub 9
spastic Tan o 9
spast aker
parapar zani g 6
ique GR,
esis a, y, ;
épid Mlin 7
associat Jou 1
émiq gi N, 1
ed with rnal 9
ue, Rosli :
chronic of 9 2
“Kon ng
cyanide Tro 4; 2
zo” H,
intoxicat pica 4 5
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